Tag: myocardial infarction

Categories : Cardiovascular Disease HIVTags :

People with HIV and Hepatitis C Have Increased Heart Attack Risk

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As people with HIV age, their risk of myocardial infarction increases far more if they also have untreated hepatitis C virus, according to new research published today in the Journal of the American Heart Association.

According to the findings, even with antiretroviral therapy (ART), the risk of myocardial infarction (MI) among people with HIV is at least 50% higher than people without HIV. This new study evaluated if people with HIV who also have hepatitis C have a higher risk of MI.

“HIV and hepatitis C coinfection occurs because they share a transmission route – both viruses may be transmitted through blood-to-blood contact,” said Associate Professor Keri N. Althoff, PhD, MPH, senior author of the study. “Due in part to the inflammation from the chronic immune activation of two viral infections, we hypothesised that people with HIV and hepatitis C would have a higher risk of heart attack as they aged compared to those with HIV alone.”

Researchers analysed health information for 23 361 people with HIV in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) between 2000–2017 started on antiretroviral treatment for HIV, median age 45 at enrolment. One in 5 study participants (4677) were also positive for hepatitis C. During a median follow-up of about 4 years, the researchers compared the occurrence of a heart attack between the HIV-only and the HIV-hepatitis C co-infected groups as a whole, and by each decade of age.

The analysis found:

  • With each decade of increasing age, MI incidence increased 30% in people with HIV alone and 85% in those who were also positive for hepatitis C.
  • The risk of heart attack increased in participants who also had traditional heart disease risk factors such as high blood pressure (more than 3 times), smoking (90%) and Type 2 diabetes (46%).
  • The risk of heart attack was also higher (40%) in participants with certain HIV-related factors such as low levels of CD4 immune cells (200 cells/mm3, signalling greater immune dysfunction) and 45% in those who took protease inhibitors (one type of ART linked to metabolic conditions).

“People who are living with HIV or hepatitis C should ask their doctor about treatment options for the viruses and other ways to reduce their cardiovascular disease risk,” said Assistant Professor Raynell Lang, MD, MSc, lead study author.

“Several mechanisms may be involved in the increased heart attack risk among co-infected patients. One contributing factor may be the inflammation associated with having two chronic viral infections,” A/Prof Lang said. “There also may be differences in risk factors for cardiovascular disease and non-medical factors that influence health among people with HIV and hepatitis C that plays a role in the increased risk.”

“Our findings suggest that HIV and hepatitis C co-infections need more research, which may inform future treatment guidelines and standards of care,” Althoff said.

The study is limited by not having information on additional factors associated with heart attack risk such as diet, exercise or family history of chronic health conditions. Results from this study of people with HIV receiving care in North America may not be generalizable to people with HIV elsewhere. In addition, the study period included time prior to the availability of more advanced hepatitis C treatments.

“Because effective and well-tolerated hepatitis C therapy was not available during several years of our study period, we were unable to evaluate the association of treated hepatitis C infection on cardiovascular risk among people with HIV. This will be an important question to answer in future studies,” Lang said.

Source: American Heart Association

Categories : Cardiovascular DiseaseTags :

Gout Flare-ups Linked to Increased MI and Stroke Risk

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The risk of myocardial infarction (MI) and strokes temporarily increases in the four months after a gout flare, suggests a study published in the journal JAMA.

The findings showed that gout patients who suffered from an MI or stroke were twice as likely to have had a gout flare in the 60 days prior to the event, and one and a half times more likely to have a gout flare in the 61-120 days prior.

Gout is a common form of arthritis that is caused by high levels of uric acid, a chemical produced by breakdown of body tissues and present in certain foods and drinks.

At high levels, uric acid is deposited in and around joints as needle shaped urate crystals. Once released from their deposits, these crystals cause severe inflammation that manifest as joint pain, swelling, redness, and tenderness that often lasts for 1–2 weeks. These episodes, called gout flares, often recur. Inflammation is also a risk factor for heart attack and stroke.

While gout patients tend to have more cardiovascular risk factors, there have been no previous studies about whether gout flares are linked with an increased risk of MI and stroke.

To address this, the team used data from 62 574 patients with gout treated in the NHS. Of these, 10 475 experienced heart attack or stroke after the diagnosis of gout, while matched controls did not experience such events. They evaluated the association between heart attacks or strokes and recent gout flares and adjusted these results for possible confounding factors. They found that gout patients who suffered an MI or stroke were twice as likely to have had a gout flare in the 60 days prior to the event, and one and a half times more likely to have a gout flare in the preceding 61–120 days.

They found a similar high rate of MI or stroke in the 0–60 and 61–120 days after gout flares compared with other time periods, when they used information from only patients who consulted for a gout flare and also experienced either MI or stroke. This further strengthened the finding that gout flares are associated with a transient increase in cardiovascular events following flares. The increased odds and rates persisted when people with pre-existing heart disease or stroke before their gout diagnosis were excluded, and when shorter exposure periods such as 0-15 and 16-30 days prior to MI or stroke, were considered.

Gout patients who died from a MI or stroke had over four times the odds of experiencing a gout flare in the preceding 0-60 days and over twice the odds of gout flare in the preceding 61-120 days.

The study’s lead author, Professor Abhishek at the University of Nottingham, said: “This is the first study of its kind to examine whether there is an association between recent gout flares and heart attacks and strokes.

“The results show that among patients with gout, patients who experienced a heart attack or stroke had significantly increased odds of a gout flare during the preceding 120-days compared with patients who did not experience such events. These findings suggest that gout flares are associated with a transient increase in cardiovascular events following flares.

“People with recurrent gout flares should be considered for long-term treatment with urate lowering treatments such as allopurinol. This is a reliable way of removing urate crystal deposits and providing freedom from gout flares. Patients should also be considered for concurrent treatment with anti-inflammatory medicines such as colchicine for the first few months because urate lowering treatments may trigger gout flares in the short term.

“People with gout should be encouraged to adopt a healthy lifestyle with appropriate treatment of conditions such as high blood pressure, high cholesterol, obesity and diabetes to minimise their background risk of heart attack and stroke.”

Source: University of Nottingham

Categories : Cardiovascular DiseaseTags :

Beta Blockers and Antiplatelet Drugs Tied to Heat-related MI Risk

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During hot weather events, people taking beta blockers and antiplatelet medications such as aspirin could be at increased risk of a myocardial infarction (MI), amplifying the risk already present from hot weather.

A new study published in Nature Cardiovascular Research found that, among people suffering non-fatal MI associated with hot weather, a greater portion are taking these heart drugs.

“Patients taking these two medications have higher risk,” said Assistant Professor Kai Chen, first author of the study. “During heat waves, they should really take precautions.”

External environmental factors like air pollution and cold weather can trigger MIs, and there is growing evidence to suggest that hot weather can do so, too. But epidemiologists are still working to identify which groups of people are most vulnerable to these environmental extremes.

The authors looked at 2494 cases sourced from a registry, in which individuals experienced a non-fatal MI in Augsburg, Germany during the hot-weather months (May–September) between 2001 and 2014.

In previous research, they had shown that exposure to either heat or cold made heart attacks more likely, and they calculated that heat-related MI rates would rise once the planet has warmed by 2–3°C.

The current study built on that research by examining patients’ medication use prior to their MI.

They analysed the data in a way that let patients serve as their own controls, by comparing heat exposure on the day of the MI versus the same days of the week within the same month. That is, if a person had an NI on the third Thursday in June, the authors compared their temperature exposure that day to their temperature exposure on other, “control” Thursdays in June.

It turned out that users of beta-blockers or antiplatelet medications were likelier to have an MI during the hottest days compared to control days. Antiplatelet medication use was associated with a 63% increase in risk and beta-blockers with a 65% increase. People taking both drugs had a 75% higher risk. Non-users of those medications were not more likely to have a heart attack on hot days.

When researchers compared younger patients (25–59 years) to older ones (60–74 years), they found, as expected, that the younger ones were a healthier group, with lower rates of coronary heart disease. Yet younger patients taking beta-blockers and antiplatelet medications were more susceptible to heat-related heart attack than older patients, despite the older ones having more heart disease.

Another clue that these two medication types may render people more vulnerable is that, other heart medications generally didn’t show a connection to heat-related heart attacks. An exception was statins, which taken by younger people, were associated with an over threefold risk of a heart attack on hot days.

“We hypothesise that some of the medications may make it hard to regulate body temperature,” Asst Prof Chen said. He plans to find out why in future studies.

The results suggest that as climate change progresses, heart attacks might become a greater hazard to some people with cardiovascular disease.

Source: Yale School of Public Health

Categories : Cardiovascular DiseaseTags :

Study Sheds Light on Cardiac Repair after MI

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Photo from Olivier Collett on Unsplash
Photo from Olivier Collett on Unsplash

Immune response and the lymphatic system are central to cardiac repair after a heart attack, according to a study published in the Journal of Clinical Investigation. These insights into the basic mechanisms of cardiac repair pave the way towards the development of new treatments to preserve heart function.

“We found that macrophages, or immune cells that rush to the heart after a heart attack to ‘eat’ damaged or dead tissue, also induce vascular endothelial growth factor C (VEGFC) that triggers the formation of new lymphatic vessels and promotes healing,” said co-senior author Edward Thorp, PhD, from the Heart Center at Lurie Children’s and Associate Professor of Pathology and Pediatrics at Northwestern University Feinberg School of Medicine. “Our challenge now is to find a way either to administer VEGFC or to coax these macrophages to induce more VEGFC, in order to speed the heart repair process.”

People who suffer a heart attack are at high risk for heart failure, even with the advances in medications to reduce mortality. This occurs in part because some macrophages that arrive at the site of damage are proinflammatory and do not induce VEGFC.

“It is a Dr. Jekyll and Mr. Hyde scenario, with ‘good’ macrophages that induce VEGFC and the ‘bad’ ones that don’t. We need to prevent the ‘bad’ macrophages from causing further damage,” said co-senior author Guillermo Oliver, PhD, Director of Feinberg Cardiovascular and Renal Research Institute – Center for Vascular and Developmental Biology, and Professor of Medicine at Northwestern University Feinberg School of Medicine. “We are working to understand more about the progression to heart failure after a heart attack, in order to intervene early and reset the course to cardiac repair.”

Source: DICardiology

Categories : Cardiovascular DiseaseTags :

Thoracic Aorta Diameter Can Predict Cardiovascular Risk

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Anatomical model of a human heart
Photo by Robina Weermeijer on Unsplash

A new study in the journal Radiology has found that the diameter of the thoracic aorta can be a biomarker for heart attacks and other adverse cardiovascular events in women and men, and has the advantage of being simple to add on to existing screening.

The thoracic aorta is divided into an ascending aorta that rises from the left ventricle of the heart and a descending aorta in the back of the chest.

While the thoracic aorta grows with age, but changes of vessel size and structure, a phenomenon known as vascular remodelling, have a systemic nature involving haemodynamic and biological processes that are also linked to cardiovascular disease.

“While enlargement of the thoracic aorta is a frequent finding in clinical practice, few longitudinal data regarding its long-term prognosis for major cardiovascular disease outcomes at the population level exist,” said study senior author Maryam Kavousi MD, PhD, from University Medical Center Rotterdam.

Dr Kavousi and colleagues assessed these associations in 2178 participants from the population-based Rotterdam Study. Participants underwent multi-detector CT scans between 2003 and 2006 and were followed for an average of 9 years. Thoracic aorta diameters were indexed for body mass index (BMI).

Larger BMI-indexed ascending and descending thoracic aortic diameters were significantly associated with increased risk of adverse cardiovascular outcomes like stroke and death in both women and men.

“Our results suggest that imaging-based assessment of diameter of thoracic aorta can be considered as a risk marker for future cardiovascular disease,” Dr Kavousi said.

In women, greater ascending aortic diameter was associated with 33% higher cardiovascular mortality risk. There seems to be a sex difference in remodelling of the ageing aorta, with faster deterioration in women.

“Ageing could affect aortic health and structure more adversely in women than in men,” Dr Kavousi said.

The study findings suggest that cardiovascular risk assessment associated with thoracic aortic size among asymptomatic women and men could lead to effective, sex-specific prevention strategies.

“As the aortic diameter is significantly related to body size, use of aortic diameters indexed for body measurements could improve its prognostic value for cardiovascular outcomes,” Dr Kavousi said.

Measurement of thoracic aorta size is an easy addition to current screening, the researchers said. The study made use of cardiac CT scans that are already commonly used to assess coronary calcium. Thoracic aortic diameter could also be measured routinely, for example as part of CT-based lung cancer screening.

The current study was based on a single CT-based assessment of thoracic aorta among a large group of participants from the general population, followed up for nine years for incidence of cardiovascular outcomes and mortality. The researchers have recently repeated the CT-based assessment of thoracic aorta among these participants after a median of 14 years.

“This provides an exciting and unique opportunity to study sex-specific risk profiles and patterns of growth in thoracic aorta in the general population,” Dr Kavousi said.

Source: Radiological Society of North America

Categories : Cardiovascular Disease Regenerative MedicineTags :

A Review of Progress Toward Heart Muscle Regeneration

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Photo from Olivier Collett on Unsplash
Photo from Olivier Collett on Unsplash

Twenty years ago, clinicians first attempted to regenerate a failing human heart by injecting muscle myoblasts into the heart during a bypass operation. Despite high initial hopes and multiple studies since then, attempts to remuscularise an injured heart have met with little, if any, success.

Yet, there is hope that a therapy will be developed, according to experts in a Journal of the American College of Cardiology state-of-the-art review. The challenge is this: A heart attack kills heart muscle cells, leading to a scar that weakens the heart, often causing eventual heart failure. The lack of muscle repair is due to the very limited ability of mammalian heart muscle cells to proliferate, except during a brief period around birth.

In the review, the experts focus on three topics. First are several recent clinical trials with intriguing results. Second is the current trend of using cell-derived products like exosomes rather than muscle cells to treat the injured heart. For the third topic, authors discuss likely future experiments to replace a myocardial scar with heart muscle cells by ‘turning back the clock’ of the existing cardiomyocytes, rather than trying to inject exogenous cells. These efforts try to reverse the inability of mature mammalian heart muscle cells to proliferate.

Clinical trials
One of the clinical trials reviewed involved giving cardiosphere-derived cells to patients with Duchenne muscular dystrophy, which affects both heart and skeletal muscles.

Cardiosphere-derived cells are a type of heart stromal/progenitor cell that has potent immunomodulatory, antifibrotic and regenerative activity in both diseased hearts and skeletal muscle. The HOPE-2 trial gave repeated intravenous doses of cardiosphere-derived cells to patients with advanced Duchenne disease, most of whom were unable to walk. Preliminary results showed safety, as well as major improvements in heart parameters such as left ventricle ejection fraction and reduced left ventricle size.

The HOPE-2 trial evaluated a repeated sequential dosing regimen of cell therapy for any cardiac indication, evaluated intravenous cardiosphere-derived administration, and clinically benefitted Duchenne patients.

Two features of the trial may bode well: a move away from invasive cardiac-targeted cell delivery and toward easily administered intravenous cell delivery, and the use of sequential repeated cell doses.

Cell-derived products
Few cells transplanted into the heart survive, though some functional benefits in heart performance have been seen despite physical clearance of grafted cells. It could be possible that the cells were acting not as replacements but rather boosters of endogenous repair pathways through the release of a wide array of tissue-repairing biomolecules.
This led to investigation of using cell-derived products rather than transplanting cells. Most of these biomolecules – proteins and non-coding nucleic acids – are enclosed in tiny vesicles that cells release naturally. When the vesicles, including exosomes, merge into recipient cells, the biomolecules can modulate signaling pathways. Using vesicles or exosomes involves a simpler manufacturing process compared with live cells, the ability to control quality and potency, and being able to refrigerate the vesicles to make administration simpler.

An alternative approach to the vesicle cell-derived products was the finding that injected stem cells can promote cardiac repair through release of biologically active molecules acting as short-range, paracrine hormones. These molecules are distinct from the biomolecules in vesicles or exosomes.

However, before use of any of these cell-derived products for heart repair in early trials, the reviewers say, more experiments are needed in purification of the products, potential modes of delivery and the suitability of repeated doses.

Proliferation of endogenous heart cells
The final review topic looked ahead toward endogenous generation of cardiomyocytes – in other words, forcing existing native cardiomyocytes to divide, or other cells to become cardiomyocytes.

Pigs can regenerate heart muscle for only a few days after birth. But in one remarkable study, researchers injured the heart by removing part of the apex of the left ventricle one day after birth, and then induced heart attack 28 days after birth. Control pigs without the Day 1 resection showed no repair of heart attack damage at Day 56. In contrast, the pigs that had a resection one day after birth, and then had experimental heart attacks at Day 28, showed heart repair by Day 56 – notably an absence of dead heart muscle, known as an infarction. Furthermore, these pigs had more cardiomyocytes throughout their left ventricles.

This study showed that heart muscle cells in large mammals can be induced to proliferate and regenerate by inducing a heart injury at Day 1 to extend the neonatal regneration window. “If this cardiomyocyte cell-cycle activation can be activated in neonates, the same signaling pathways may be activated in adults as well,” the authors wrote, “which is highly impactful and significant.”

Another possible approach to endogenous generation is the direct programming of cardiac fibroblasts into cardiomyocytes. Inducing proliferation of cardiomyocytes will also need ways to promote growth of heart blood vessels to supply the new cardiomyocytes.

In conclusion, the authors believe that short-term approaches to clinical trials of post heart-attack therapies will use cells like cardiospheres or cell products. The longer-term approach, the reviewers said, will target “a more direct remuscularisation of the injured left ventricle by ‘turning back the clock’ of the cardiomyocyte cell-cycle or generating new cardiomyocytes from other cell types such as fibroblasts.”

“However, the efficiency and safety of these strategies, particularly their ability to generate cardiomyocytes seamlessly coupled with their native counterparts and to allow a regulation of these induced proliferative events preventing an uncontrolled and harmful cardiac growth, still need to be appropriately addressed before moving to clinical applications.”

Source: University of Alabama at Birmingham

Categories : Cardiovascular DiseaseTags :

Parental History Not The Only Premature Heart Attack Risk

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A new study has shown that, while parental history is a contributing factor, young heart attack victims are more likely to be smokers, obese, and have high blood pressure or diabetes compared to their peers.

“The findings underline the importance of preventing smoking and overweight in children and adolescents in order to reduce the likelihood of heart disease later in life,” said study author Professor Harm Wienbergen of the Bremen Institute for Heart and Circulation Research.

“Understanding the reasons for heart attacks in young adults is important from a societal perspective due to their employment and family responsibilities,” he continued. “However, there are limited data on the predictors of heart events in this group.”

The researchers compared the clinical characteristics of consecutive patients admitted to hospital with acute myocardial infarction at 45 years of age or younger against randomly selected individuals from the German population. Cases and controls were matched according to age and gender. The case-control study enrolled a total of 522 patients with 1191 matched controls from a national database.

The researchers found that the proportion of active smokers was more than three-fold higher in the young heart attack group compared to the general population (82.4% vs 24.1%). Patients were more likely to have high blood pressure (25.1% vs 0.5%), diabetes (11.7% vs 1.7%) and a parental history of premature heart attack (27.6% vs 8.1%) compared to their peers. Patients were more often obese, with a median body mass index (BMI) of 28.4 kg/m2 compared to 25.5 kg/m2 for controls. In contrast, the proportion consuming alcohol at least four times a week was higher in the general population (11.2%) compared to heart patients (7.1%).

The researchers analysed the independent risk factors for the occurrence of acute myocardial infarction at 45 years of age or younger. The analysis was adjusted for age, sex, high blood pressure, diabetes, active smoking, body mass index, alcohol consumption, years of school education, and birth in Germany.

Hypertension was associated with an 85-fold odds of a heart attack aged 45 or under. The corresponding odds of a premature heart attack associated with active smoking, diabetes mellitus, parental history and obesity (BMI 30 kg/m2 or above) were 12, 5, 3 and 2. Alcohol consumption was associated with a lower odds of heart attack at a young age with an odds ratio of 0.3.

Prof Wienbergen said: “Our study shows that smoking and metabolic factors, such as hypertension, diabetes and obesity, are strongly associated with an increased likelihood of premature acute myocardial infarction. A protective effect of moderate alcohol consumption has been described by other studies and is confirmed in the present analysis of young patients.”

He concluded: “Our study suggests that family history is not the only predisposing factor for early heart attacks. The findings add impetus to the argument that young people should be educated about why it is important to avoid smoking and have a healthy body weight.”

Source: European Society of Cardiology

Categories : Cardiovascular Disease New Compounds and TreatmentsTags :

A Treatment for Heart Attack from Spider Venom

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Photo by Adrián Valverde on Unsplash
Photo by Adrián Valverde on Unsplash

A protein found in the venom of one of the world’s deadliest spiders has been shown to preserve heart cells, and could be developed into a potentially life-saving treatment for heart attack victims.

A drug candidate developed from a molecule found in the venom of the Fraser Island (K’gari) funnel web spider can prevent damage caused by a heart attack and extend the life of donor hearts used for organ transplants. This would not be the first investigation into a clinical application for spider venom, however. Tarantula spider venom has also been investigated as a potent anaesthetic.

The discovery was made by a team led by Dr Nathan Palpant and Professor Glenn King from The University of Queensland (UQ) and Professor Peter Macdonald from the Victor Chang Cardiac Research Institute.

Dr Palpant, from UQ’s Institute for Molecular Bioscience (IMB), said the drug candidate worked by stopping a ‘death signal’ sent from the heart in the wake of an attack.

“After a heart attack, blood flow to the heart is reduced, resulting in a lack of oxygen to heart muscle,” Dr Palpant said. “The lack of oxygen causes the cell environment to become acidic, which combine to send a message for heart cells to die.

“Despite decades of research, no one has been able to develop a drug that stops this death signal in heart cells, which is one of the reasons why heart disease continues to be the leading cause of death in the world.”

Using beating human heart cells exposed to heart attack stresses, Dr Palpant tested the drug candidate, a protein called Hi1a, to see if the drug improved the cells’ survival.

“The Hi1a protein from spider venom blocks acid-sensing ion channels in the heart, so the death message is blocked, cell death is reduced, and we see improved heart cell survival.”

At present, there are no drugs in clinical use that prevent the damage caused by heart attacks.

Professor Macdonald of Victor Chang Cardiac Research Institute said that this incredible result had been decades in the making.

“This will not only help the hundreds of thousands of people who have a heart attack every year around the world, it could also increase the number and quality of donor hearts, which will give hope to those waiting on the transplant list,” said Professor MacDonald, who is also a senior cardiologist at St Vincent’s Hospital in Sydney.

“The survival of heart cells is vital in heart transplants — treating hearts with Hi1a and reducing cell death will increase how far the heart can be transported and improve the likelihood of a successful transplant,” added Prof MacDonald. “Usually, if the donor heart has stopped beating for more than 30 minutes before retrieval, the heart can’t be used — even if we can buy an extra 10 minutes, that could make the difference between someone having a heart and someone missing out. For people who are literally on death’s door, this could be life-changing.”

The discovery builds on earlier work by Professor King, who identified a small protein in the venom of the Fraser Island (K’gari) funnel-web spider that was shown to markedly improve recovery from stroke.

“We discovered this small protein, Hi1a, amazingly reduces damage to the brain even when it is given up to eight hours after stroke onset,” Professor King said.

“It made sense to also test Hi1a on heart cells, because like the brain, the heart is one of the most sensitive organs in the body to the loss of blood flow and lack of oxygen.

“For heart attack victims, our vision for the future is that Hi1a could be administered by first responders in the ambulance, which would really change the health outcomes of heart disease.”

“This is particularly important in rural and remote parts of Australia where patients and treating hospitals can be long distances apart — and when every second counts.”

Also, this could help for the transfer of donor hearts for cardiac transplantation — allowing these donor hearts to be transported over longer distances and therefore increasing the network of available donors and recipients.

The protein has been tested in human heart cells, and the team are aiming for human clinical trials for both stroke and heart disease within 2-3 years.

Source: ScienceDaily

Journal information: Meredith A. Redd, et al. Therapeutic Inhibition of Acid Sensing Ion Channel 1a Recovers Heart Function After Ischemia-Reperfusion Injury. Circulation, 2021; DOI: 10.1161/CIRCULATIONAHA.121.054360

Categories : Cardiovascular Disease COVIDTags :

Drop in Heart Attacks Linked to COVID Pandemic

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A sharp drop in heart attacks in Finland last year seems to be a result of the COVID pandemic, doctors believe.

Cardiologist Mika Laine noticed a roughly 30 per cent reduction in the number of patients suffering myocardial infarction at Helsinki University Central Hospital in April and May 2020. But what was even more surprising was that this was not an isolated occurrence.

“When we started to study this further, we noticed that exactly the same phenomenon happened everywhere else in Finland and also in other countries in Europe and in the United States. So it was a kind of global phenomenon that happened during the COVID pandemic,” he told Euronews.

What was behind the drop?

Dr Laine is of the opinion that the fall in heart attack patient numbers results from changes made in response to the COVID outbreak.

“We have the exact same genes that we had a year ago, two years ago. So it has to be something in the environment that has changed,” he said. One major factor could be the massive global shift to remote working for many people, as a result of the lockdowns.

“People are at home, they are less stressed because they don’t need to go through morning traffic, hurry to work and so forth,” Dr Laine added.

EU Science Hub data shows that even before the pandemic, Finns worked remotely more than almost any other EU country. Last May, EU labour research body Eurofound revealed that Finnish workers made the fastest switch to teleworking in the EU, with nearly 60 per cent switching over.

“We also see this decrease in those people who are retired, who don’t go to work, so it cannot be just because you’re commuting,” said Dr Laine.
He however cautioned that there could be other factors behind the fall in heart attack patients.

Was there a real fall in heart attacks in 2020?

“We know that many people stopped smoking because smoking was associated with severe COVID mortality,” he said.

Better air quality in urban areas as a result of the lockdown could be another cause, Laine said, since airborne particles are known to be a risk factor for heart disease.

However not all are convinced that the pandemic had a positive impact on patients with all types of heart conditions.

Research published in the Journal of the American College of Cardiology in January found that, during the early phase of the pandemic, deaths due to ischaemic heart disease and hypertensive diseases increased in some parts of the US. Some patients may have died as a result of avoiding hospital visits due to infection fears, the researchers noted. 

A temporary or permanent effect?

With Finland, however,Dr Laine believes that was not the case.

“We haven’t seen any increase in mortality in cardiac diseases and so currently we think that it’s a true decrease in the number of cases and not because patients are not seeking help,” he said. “People were not dying at home to myocardial infarction”.

According to Dr Laine, the number of heart attack patients in Finland remains about 5 per cent lower than average, despite the easing of COVID restrictions.

“I think this is a typical example that environmental factors can have profound effects on myocardial infarction. And I think it’s motivating us to change our lifestyle healthier,” Dr Laine said.

Source: EuroNews

Categories : Cardiovascular Disease New Compounds and TreatmentsTags :

Averting Heart Failure by Shutting Down a Heart Protein

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Photo from Olivier Collett on Unsplash
Photo from Olivier Collett on Unsplash

Shutting down a protein found in cardiac muscle could be a new mechanism to treat post-heart attack heart failure, according to research led by the University of Cambridge.

New drugs are needed to improve the heart’s pumping ability after damage from a heart attack. Drugs that strengthen the contraction of failing heart muscle have been deemed unsafe, leaving a gap in the heart attack and heart failure armamentarium.

Researchers now believe that they might have identified a new drug target—a protein called MARK4.

In research funded by the British Heart Foundation (BHF), Cambridge scientists found levels of MARK4 were elevated in mouse hearts after a heart attack. When they compared mice with and without MARK4 in the heart, they found hearts lacking the protein pumped blood 57% more efficiently. This protective effect was seen 24 hours after a heart attack and persisted over the entire follow-up period of four weeks.

The team was first in identifying that MARK4 fine-tunes a structural network within the heart muscle cell—called the microtubule network—that attaches to the machinery governing heart muscle cells contraction and relaxation. When MARK4 levels were increased after a heart attack, microtubules were tightly anchored onto the contractile machinery in the heart, increasing resistance and hindering normal function. When MARK4 levels were reduced, microtubules were loosely anchored, making contraction and relaxation easier.

Following a heart attack the speed of contraction in MARK4-lacking muscle cells increased by 42 percent and the speed of relaxation increased by 47 percent, compared to muscle cells from mice that had the MARK4 protein. They were also almost on par with healthy heart muscle performance, attesting to the power of reducing MARK4.

Based on these findings, the researchers suggested that drugs to switch off MARK4 could be a new way to improve recovery and help the heart to pump blood more efficiently in people with failing hearts.

Dr Xuan Li, BHF Intermediate Research Fellow at University of Cambridge BHF Centre of Research Excellence, said: “After years of research we’ve revealed an entirely new and promising way that could help the recovery of failing hearts.

“It’s early days, and we now need to test the longer-term effects of switching off MARK4. But if drugs to do that prove successful, the life-changing benefits could be seen in people with other types of heart disease as well as those who’ve had a heart attack and developed heart failure.”

Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation, said: “Heart attacks are a major cause of disability worldwide—people who’ve had a major heart attack are at much greater risk of developing chronic heart failure. There are around 920 000 people living with heart failure in the UK, and we desperately need drugs to drastically improve the heart’s function in these patients.

“These findings are a positive step forward. Further research is needed to refine and test drugs that can target MARK4 before we’ll see them given to people who’ve had a heart attack and develop heart failure.”

Source: University of Cambridge