A groundbreaking study conducted a comparison of arterial stiffness between participants before and after contracting COVID-19.
New research indicates that even mild instances of COVID-19 can lead to lasting harm to cardiovascular health.
The study is the first comparison of levels of arterial stiffness before and after a COVID-19 infection, a parameter closely tied to the aging process and performance of our arteries. The lingering effects of a COVID-19 infection, often referred to as long COVID, are connected with a heightened risk of cardiovascular disease, dementia, and in severe scenarios, death.
An international team of scientists was able to do this research using baseline measurements from a group of participants involved in a separate study that began pre-pandemic, also investigating arterial stiffness.
In those who had been diagnosed with mild COVID-19, artery and central cardiovascular function were affected by the disease two to three months after infection. Side effects include stiffer and more dysfunctional arteries that could lead to cardiovascular disease development.
The paper, published in the Journal of Clinical Medicine, revealed age and time from COVID infection are associated with increased aging of the arteries.
Co-author, Dr Maria Perissiou from the University of Portsmouth’s School of Sport, Health & Exercise Science, said: “We were surprised to observe such a decline in vascular health, which deteriorated even further with time since COVID-19 infection. Usually, you’d expect inflammation to decrease with time after infection, and for all the physiological functions to go back to normal or a healthy level.
“We can only speculate on what causes this phenomenon without further investigation, but emerging evidence suggests that it stems from COVID-19 triggering the auto-immune process that leads to vasculature deterioration.”
While COVID-19 has been associated with a type of acute heart failure and vascular dysfunction, the long-term consequences of the disease on vascular health still need to be explored.
The study was part of the University of Split’s NormPreven project funded by the Croatian Science Foundation, and the team formation was facilitated by EU COST VascAgeNet action.
Participants were monitored between October 2019 and April 2022 in the Laboratory for Vascular Aging at the University of Split School of Medicine.
Most were young, less than 40 years old, and healthy. Only nine percent of the group had high blood pressure, and none had high cholesterol. Two were diabetic, and 78 percent did not smoke. The group was also almost an even split between males (56 percent) and females (44 percent).
Professor Ana Jeroncic from the University of Split, who led the study, said: “Given the number of people infected with COVID-19 worldwide, the fact that infection can have harmful effects on cardiovascular health in young people who had a mild form of the disease warrants close monitoring.
“The question remains as to whether this harmful effect is irreversible or permanent, and if not, for how long it lasts.”
Dr. Perissiou added: “This study, while small, does support the prediction amongst vascular physiologists that we’ll have an increase in cardiovascular disease in the future as a result of COVID-19 infections. But we have to consider what other variables would have contributed to this increase.”
The paper concludes the results have important implications for understanding the long-term cardiovascular consequences of COVID-19 infection and may guide prevention and management strategies for associated vascular disease.
However, it recommends further research is needed to strengthen our understanding of causes and contributing factors.
Reference: “Long-Term Adverse Effects of Mild COVID-19 Disease on Arterial Stiffness, and Systemic and Central Hemodynamics: A Pre-Post Study” by Mario Podrug, Pjero Koren, Edita Dražić Maras, Josip Podrug, Viktor Čulić, Maria Perissiou, Rosa Maria Bruno, Ivana Mudnić, Mladen Boban and Ana Jerončić, 8 March 2023, Journal of Clinical Medicine. DOI: 10.3390/jcm12062123
A small trial has found that hyperbaric oxygen therapy (HBOT) may help restore proper heart function in patients with post-COVID syndrome, with participants in the HBOT group experiencing a significant increase in global longitudinal strain (GLS), an indicator of heart function.
A small randomized trial in patients with post-COVID syndrome has found that hyperbaric oxygen therapy promotes the restoration of the heart’s ability to contract properly. The research is presented at EACVI 2023, a scientific congress of the European Society of Cardiology (ESC).[1]
“The study suggests that hyperbaric oxygen therapy can be beneficial in patients with long COVID,” said study author Professor Marina Leitman of the Sackler School of Medicine, Tel Aviv University and Shamir Medical Centre, Be’er Ya’akov, Israel. “We used a sensitive measure of cardiac function which is not routinely performed in all centers. More studies are needed to determine which patients will benefit the most, but it may be that all long COVID patients should have an assessment of global longitudinal strain and be offered hyperbaric oxygen therapy if heart function is reduced.”
Most COVID-19 sufferers fully recover, but after the initial illness approximately 10–20% of patients develop long COVID, also called post-COVID condition or syndrome.[2] Symptoms include shortness of breath, fatigue, cough, chest pain, rapid or irregular heartbeats, body aches, rashes, loss of taste or smell, nausea, vomiting, diarrhea, headache, dizziness, insomnia, brain fog, depression and anxiety. Patients with post-COVID syndrome may also develop cardiac dysfunction and are at increased risk of a range of cardiovascular disorders.[3]
This randomized controlled double-blind trial evaluated the effect of hyperbaric oxygen therapy (HBOT) on the cardiac function of long COVID patients. HBOT involves inhalation of 100% pure oxygen at high pressure to increase delivery to the body’s tissues, which is particularly beneficial for tissues that are starved of oxygen due to injury or inflammation. HBOT is an established treatment for non-healing wounds, decompression sickness in divers, carbon monoxide poisoning, radiation injury, and certain types of infections
The study enrolled 60 post-COVID syndrome patients with ongoing symptoms for at least three months after having mild to moderate symptomatic COVID-19 confirmed by a PCR test. Both hospitalized and non-hospitalized patients were included. Severe COVID cases were excluded. Patients were randomized to HBOT or a sham procedure in a 1:1 ratio. Each patient had five sessions per week over eight weeks, for a total of 40 sessions. The HBOT group received 100% oxygen through a mask at a pressure of 2 atmospheres for 90 minutes, with 5 minute air breaks every 20 minutes. The sham group breathed 21% oxygen by mask at 1 atmosphere for 90 minutes. All participants underwent echocardiography at baseline (before the first session) and 1 to 3 weeks after the last session.
Echocardiography was used to assess left ventricular global longitudinal strain (GLS), which is a measure of the heart’s ability to contract and relax lengthwise. It indicates how well the heart is functioning and can help detect early signs of heart disease. A healthy heart will have a GLS value of around -20% which means that the heart muscle is able to properly contract and relax in the longitudinal direction. Reduced GLS is an early marker that the heart is not able to contract and relax effectively.
At baseline, nearly half of study participants (29 out of 60; 48%) had reduced GLS. Of those, 13 (43%) and 16 (53%) were in the sham and HBOT groups, respectively. The average GLS at baseline across all participants was -17.8%. In the HBOT group, GLS significantly increased from -17.8% at baseline to -20.2% after the intervention (p=0.0001). In the sham group, GLS was -17.8% at baseline and -19.1% after the sessions, with no statistically significant difference between the two measurements.
Professor Leitman said: “It was notable that almost half of long COVID patients had impaired cardiac function at baseline according to GLS despite all participants having a normal ejection fraction, which is the standard method for measuring the heart’s ability to contract. This means that ejection fraction is not sensitive enough to identify long COVID patients with reduced heart function.”
She concluded: “The findings suggest that HBOT promotes recovery of cardiac function in patients with post-COVID syndrome. More research is needed to collect long-term results and determine the optimal number of sessions for maximum therapeutic effect.”
What the research shows about risks of myocarditis from COVID vaccines versus risks of heart damage from COVID – two pediatric cardiologists explain how to parse the data.
Rare cases of myocarditis have been reported after COVID-19 vaccination, but the risk is higher after infection, and the prognosis is better following vaccine-related myocarditis. The decision to vaccinate should consider factors like patient age, health problems, and community COVID-19 rates.
Soon after the first COVID-19 vaccines appeared in 2021, reports of rare cases of heart inflammation, or myocarditis, began to surface.
In most instances, the myocarditis has been mild and responded well to treatment, though up to four potentially mRNA vaccine-related deaths from myocarditis in adults have been reportedworldwide. No known verified deaths of children have been reported based on publicly available data. The exact number remains a topic of very heated debate because of variability in the reporting of possible myocarditis-related deaths.
Studies have largely confirmed that the overall myocarditis risk is significantly higher after an actual COVID-19 infection compared with vaccination, and that the prognosis following myocarditis due to the vaccine is better than from infection. The specific myocarditis risk varies by age and has been debated because of differing views among a small group of physicians related to risk tolerance and support for or against COVID-19 immunization for specific age groups.
As pediatric cardiologists, we specialize in heart issues relevant to kids of all ages. We believe it is important to weigh the risk of myocarditis caused by COVID-19 immunization against not only viral myocarditis from COVID-19, but also all the other complications that COVID-19 can lead to.
Comparing risks of myocarditis from severe disease versus COVID-19 vaccination or infection is difficult to do well, and debatecontinues over which of those outcomes poses a higher risk.
Myocarditis is any condition that causes heart inflammation. A closely related condition called pericarditis refers to inflammation of the outside lining of the heart. For the purpose of this article, we focus primarily on myocarditis, since it has the potential for being a more severe condition. Most cases of myocarditis are caused by infections, particularly viral ones.
Myocarditis can be confirmed by a combination of an electrocardiogram, an ultrasound heart picture called an echocardiogram, and some blood testing. When it is available, cardiac magnetic resonance imaging, or MRI, is the most accurate method to diagnose myocarditis that doesn’t involve an invasive procedure.
A mistaken assumption is that all myocarditis is severe, since it implies damage to the heart. However, mild cases in which there is very little swelling and only temporary damage to the heart are more common than severe cases that require a machine to support heart function.
Symptoms of myocarditis include chest pain and shortness of breath.
The challenge of parsing risks of myocarditis from viral infection compared with COVID-19 vaccination is due in part to the difficulty of establishing a diagnosis of myocarditis and its population rates accurately.
That vetted data is then reported in more robust databases like the Vaccine Safety Datalink. A very small number of the myocarditis events following COVID-19 vaccination have resulted in significant long-term consequences like heart rhythm troubles. However, such cases do not reflect the majority.
Thankfully, severe myocarditis after mRNA vaccination for COVID-19 is extremely rare. A 2021 study from Nordic scholars, which looked at comparative risks of myocarditis and heart arrhythmia in patients who experienced myocarditis after COVID-19 infection versus immunization found that the risks vary significantly by age group.
This has been touted as a reason not to vaccinate healthy young men against COVID-19. The follow-up study, however, found that the comparative risks of negative outcomes were worse from myocarditis from COVID-19 infection and other viral myocarditis than from vaccination in all patients older than 12 years of age.
And it’s worth noting that, as of mid-March 2023, the U.S. still leads the world in COVID-19 hospitalizations.
A survey of all currently available research reveals that the risk of myocarditis after COVID-19 vaccination is highest in young men between the ages of 18 and 39 and older teen boys in the age range of 12 to 17, with the highest risk after the second dose of vaccine. The cause appears to be related to how the immune system processes the mRNA and sometimes generates an excessive immune response.
Myocarditis risk related to COVID-19 immunization is markedly lower in children younger than 12 years of age and much lower in adult males older than 50. The risk of severe disease from COVID-19, particularly in those older than 50 years, has been far higher throughout the pandemic than the risk of myocarditis from COVID-19 vaccination. The risk of vaccination myocarditis is uniformly lower in girls than in boys.
Infants younger than 6 months can get immunity only from their mother’s antibodies unless they are exposed to COVID-19 themselves, as vaccines for this age group are not available.
While the risks of myocarditis have been highest in teen boys and young men regardless of cause, the severity and outcome of myocarditis was much worse at the 90-day mark when it stemmed from COVID-19 infection or other viral diseases. This mirrors our team’s research on this same topic.
This discussion also doesn’t take into account the clot and heart attack risks from COVID-19 itself. Because COVID-19 damages blood vessels in all parts of the body, some organ damage such as kidney failure, blood clots, heart attacks and strokes can occur.
We recognize a need for more research into how people fare over the medium and long terms following a case of immunization-related myocarditis. This is why research is ongoing, and researchers like us are committed to following the data for years to come.
The primary risk that COVID-19 presents now to children is long COVID, followed by the risk of severe disease. The estimated percentage of children acquiring long COVID is still being debated, but the symptoms from long COVID can be extraordinarily debilitating. These include severe fatigue, brain fog, sleep disturbance, dizziness, nerve pain and more.
Many children with long COVID-19 report lingering fatigue and frequent headaches.
We believe that the decision of whether to vaccinate against COVID-19 should be based upon the patient’s age, other health problems, relative risk from vaccines, how much and what type of COVID-19 is in your community, and the patient’s and family’s preference.
Two ways that have been suggested by the CDC and the Public Health Agency of Canada to decrease the risk of COVID-19 vaccine myocarditis are to opt for Pfizer and to space your doses out by at least eight weeks. This is because Pfizer has slightly lower rates of myocarditis than Moderna.
Thankfully kids have fared far better from COVID-19 infection than adults. The primary risks of severe COVID-19 for children are among babies and infants, as well as children with health problems that put them at high risk, children with the most significant types of congenital heart disease or those with other medically complex conditions. Children in those groups derive the most benefit from the primary COVID-19 vaccine series; therefore, the decision to vaccinate in their case should be easier.
Informed consent that comes with vaccination should involve discussion of infection risks. The risk of immunization will never be zero because of variability in immune system responses; therefore, making the decision should always involve considering the most-up-to date information available.
Results also suggest the diabetes risk persists across COVID-19 variants, and that upfront vaccination may help to reduce risk of post-infection diabetes.
Investigators in the Smidt Heart Institute at Cedars-Sinai have confirmed that people who have had COVID-19 have an increased risk for new-onset diabetes—the most significant contributor to cardiovascular disease.
“Our results verify that the risk of developing Type 2 diabetes after a COVID-19 infection was not just an early observation but, in fact, a real risk that has, unfortunately, persisted through the Omicron era,” said Alan Kwan, MD, first and corresponding author of the study and a cardiovascular physician in the Smidt Heart Institute at Cedars-Sinai.
The trend, Kwan says, is concerning because most people in the United States will eventually experience a COVID-19 infection. “This research study helps us understand—and better prepare for—the post-COVID-19 era of cardiovascular risk,” Kwan said.
The findings, published today in the journal JAMA Network Open, also suggest that the risk of Type 2 diabetes appears lower in individuals who were already vaccinated against COVID-19 by the time they were infected.
To determine the rising rates of diabetes, investigators evaluated medical records from 23,709 adult patients who had at least one documented COVID-19 infection and were treated within the Cedars-Sinai Health System in Los Angeles from 2020-2022. The average patient was 47 years old, and 54% of subjects were female.
Within the study time frame:
“These results suggest that COVID-19 vaccination prior to infection may provide a protective effect against diabetes risk,” said Kwan. “Although further studies are needed to validate this hypothesis, we remain steadfast in our belief that COVID-19 vaccination remains an important tool in protecting against COVID-19 and the still-uncertain risks that people may experience during the post-infection period.”
Susan Cheng, MD, MPH, senior author of the study, professor of Cardiology, and director for Cardiovascular Population Sciences in the Smidt Heart Institute, says these findings broaden the medical field’s understanding of the effects of COVID-19 on the body, while simultaneously unearthing yet-to-be-answered questions.
“Although we don’t yet know for certain, the trends and patterns that we see in the data suggest that COVID-19 infection could be acting in certain settings like a disease accelerator, amplifying risk for a diagnosis that individuals might have otherwise received later in life,” said Cheng, the Erika J. Glazer Chair in Women’s Cardiovascular Health and Population Science. “So, it could be that instead of being diagnosed with diabetes by age 65, a person with preexisting risk for diabetes might—after a COVID-19 infection—be more likely to develop diabetes by age 45 or 55.”
Diabetes disrupts normal metabolism and metabolic processes, preventing the pancreas from producing enough insulin, a hormone that helps regulate blood levels of glucose and amino acids. Because diabetes can damage vital organs and blood vessels, people with diabetes are at higher risk for heart attack and stroke.
The disease affects an estimated 26 million people in the United States.
This research, Kwan says, is one piece of the puzzle that will help researchers understand how to prevent metabolic as well as cardiovascular disease risk in the future.
“As we learn how to live with COVID-19, we also have to be prepared to recognize and treat the various conditions linked to its aftereffects,” said Kwan. “Our ultimate goal—with every research study we conduct—is to find ways to keep people healthy and able to engage in their everyday activities and lives.”
Reference: “Association of COVID-19 Vaccination With Risk for Incident Diabetes After COVID-19 Infection” by Alan C. Kwan, MD, MSc; Joseph E. Ebinger, MD; Patrick Botting, MSPH; Jesse Navarrette, MPA; Brian Claggett, PhD and Susan Cheng, MD, MPH, MMSc, 14 February 2023, JAMA Network Open. DOI: 10.1001/jamanetworkopen.2022.55965
Experiencing lasting symptoms months after catching COVID-19, also known as long COVID, was found to more than double a person’s likelihood of developing cardiovascular issues. This is according to a study that will be presented at the American College of Cardiology’s Annual Scientific Session Together With the World Congress of Cardiology.
The study—a systematic literature review and meta-analysis of 11 major studies involving a total of 5.8 million people—represents the most comprehensive effort to date to examine cardiovascular complications from long COVID. Estimates of the number of people affected by long COVID vary substantially, but recent surveys suggest about 1 in 7 people in the U.S. have experienced long COVID.
Researchers found consistent evidence that individuals with long COVID were significantly more likely than those who never had COVID-19 to experience symptoms associated with heart problems such as chest pain, shortness of breath, palpitations, and fatigue, and more likely to show markers of heart disease or elevated cardiovascular risk in medical imaging and diagnostic tests.
“COVID-19 is more than a simple respiratory disease—it is a syndrome that can affect the heart,” said Joanna Lee, a medical student at David Tvildiani Medical University in Tbilisi, Georgia, scholar at the Global Remote Research Scholars Program (GRRSP) and the study’s lead author. “Clinicians should be aware that cardiac complications can exist and investigate further if a patient complains of these symptoms, even a long time after contracting COVID-19. For patients, if you had COVID-19 and you continue to have difficulty breathing or any kind of new heart problems, you should go to the doctor and get it checked out.”
GRRSP researchers systematically screened a total of 982 studies published between 2020-2022 and selected 74 studies for a thorough review. Of these, they identified 11 studies that included data on cardiovascular outcomes among people with long COVID as well as a control group of participants who never had COVID-19. Of more than 5.8 million participants included across the 11 studies, almost 450,000 experienced cardiac complications. Among those with long COVID, the rate of cardiac complications was 2.3-2.5 times higher compared with those in the control group.
“Coordinated efforts among primary care providers, emergency room staff, and cardiologists could help with early detection and mitigation of cardiac complications among long COVID patients,” Lee said.
There is no single definition for long COVID. For this study, researchers defined long COVID as symptoms persisting for at least four weeks and occurring at least two months after the initial COVID-19 infection. Patients with preexisting cardiovascular disease were included in the samples, but their symptoms were only counted as cardiovascular complications of long COVID if they emerged after the COVID-19 infection. For example, if someone with a history of ischemic heart disease was diagnosed with new onset atrial fibrillation post-COVID-19, they were counted.
Although the study did not investigate the possible biological mechanisms involved in the association between long COVID and heart complications, researchers said that chronic inflammation, which has been documented by persistently elevated inflammatory markers in people with long COVID, could be a factor. They added that a high level of variability between studies in terms of population and data collection methods also limited the ability to draw definitive conclusions—a common limitation with COVID-19-related studies, given the lack of long-term data.
Further analyses to determine whether people with preexisting cardiovascular disease may face different cardiovascular risks related to long COVID as compared with the general population are planned, researchers said.
Lee will present the study, “Cardiac Complications among Long Covid Patients: A Systematic Review and Meta-Analysis,” on Monday, March 6, at 11 a.m. CT / 17:00 UTC in Room 357.
Analyzing the most extensive datasets in the United States, researchers from the Icahn School of Medicine at Mount Sinai have revealed that vaccination against COVID-19 is associated with fewer heart attacks, strokes, and other cardiovascular issues among people who were infected with SARS-CoV-2, the virus that causes COVID-19.
The research letter, “Impact of Vaccination on Major Adverse Cardiovascular Events in Patients with COVID-19 Infection,” was published on February 20 in the Journal of the American College of Cardiology.
In addition, the research will be presented in a poster session in New Orleans, LA, at the American College of Cardiology’s 72nd Annual Scientific Session Together With World Heart Federation’s World Congress of Cardiology.
It is the first study to examine both full and partial vaccination and the link to major adverse cardiac events (MACE) in the United States, confirming similar analyses performed previously using the Korean COVID-19 registry. Researchers used the National COVID Cohort Collaborative (N3C) database, the largest national comprehensive database on COVID-19. Since its inception in 2020, the N3C has continuously collected and harmonized data from electronic health records of institutions across the country. Included in this study were 1,934,294 patients, 217,843 of whom received mRNA vaccine formulations by Pfizer-BioNTech or Moderna or viral vector technology by Johnson & Johnson. Cox proportional hazards, a statistical technique, was implemented to assess vaccination association with MACE.
“We sought to clarify the impact of previous vaccination on cardiovascular events among people who develop COVID-19 and found that, particularly among those with comorbidities, such as previous MACE, type 2 diabetes, high cholesterol, liver disease, and obesity, there is an association with a lower risk of complications. While we cannot attribute causality, it is supportive evidence that vaccination may have beneficial effects on a variety of post-COVID-19 complications,” said senior author Girish N. Nadkarni, MD, MPH, Irene and Dr. Arthur M. Fishberg Professor of Medicine at Icahn Mount Sinai, Director of The Charles Bronfman Institute of Personalized Medicine, and System Chief, Division of Data Driven and Digital Medicine (D3M), Department of Medicine.
“To our surprise, even partial vaccination was associated with lower risk of adverse cardiovascular events,” said first study author Joy Jiang, an MD/PhD candidate in the lab of Dr. Nadkarni. “Given the magnitude of SARS-CoV-2 infection worldwide, we hope our findings could help improve vaccination rates, especially in individuals with coexisting conditions.”
Further work will be necessary to elucidate the mechanisms involved from an immunological perspective and clarify the role of SARS-CoV-2 subtypes and reinfections in their relationship to the risk of MACE.
Reference: “Impact of Vaccination on Major Adverse Cardiovascular Events in Patients With COVID-19 Infection” by Joy Jiang, Lili Chan, Justin Kauffman, Jagat Narula, Alexander W. Charney, Wonsuk Oh, GIrish Nadkarni and on behalf of the N3C Consortium, 10 February 2023, Journal of the American College of Cardiology. DOI: 10.1016/j.jacc.2022.12.006
Additional co-authors are Lili Chan, MD, MS; Justin Kauffman, BS; Jagat Narula, MD, PhD; Alexander W. Charney, MD, PhD; and Wonsuk Oh, PhD, all from Icahn Mount Sinai.
The work was supported, in part, by funds from the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health, grant numbers K23DK124645 and T32DK007757, and by the TL1 Career Development Award, 1TL1TR004420-01.
The Mount Sinai Hospital / Mount Sinai School of Medicine
According to a study recently published in Nature Medicine and supported by the British Heart Foundation (BHF) Data Science Centre at Health Data Research UK, approximately 500,000 individuals were unable to initiate treatment with blood pressure-lowering medications during the Covid-19 pandemic.
The researchers warn that the delay in starting vital blood pressure-lowering medications could result in thousands of preventable heart attacks or strokes, as these medications play a crucial role in preventing deadly heart and circulatory diseases.
Using data on routinely dispensed prescriptions in England, Scotland, and Wales, scientists found that 491,306 fewer people than expected started taking blood pressure-lowering medication between March 2020 and the end of July 2021.
If these individuals’ high blood pressure remains untreated over their lifetime, the team estimate that this could lead to more than 13,500 additional cardiovascular events, including over 2,000 heart attacks and 3,000 strokes.
These findings highlight an important opportunity for the NHS to identify and treat people who should have started taking medicines to reduce their risk of conditions including heart attack and stroke.
Lead author Professor Reecha Sofat, Associate Director at the BHF Data Science Centre, Breckenridge Chair of Clinical Pharmacology at the University of Liverpool, warned:
“Measures to prevent infection spread were necessary and undoubtedly saved lives. The NHS has already taken important and positive steps toward identifying people with high blood pressure as early as possible. However, we need this focus to be sustained in the long-term to prevent any increase in heart attacks and strokes which will add to a healthcare system already under extreme pressure.”
To understand more about the impact of the Covid-19 pandemic on the management of risk factors for heart and circulatory diseases, the researchers analyzed 1.32 billion records of medications dispensed to 15.8 million people in England, Scotland, and Wales between 1st April 2018 and 31st July 2021.
This showed that, by the first half of 2021, on average, 27,070 fewer people started taking blood pressure-lowering medication each month between compared with 2019. In the same period, they found that 16,744 fewer people started taking medication to reduce levels of fat or cholesterol in their blood each month.
Identifying the individuals who missed starting medication as soon as possible will be critical to reducing their cardiovascular risk. The team believes that identifying those who missed out on blood pressure treatment within five years would reduce the total number of cardiovascular events to just over 2,700.
This is the first time that medicines data has been used to follow changes in the day-to-day management of chronic conditions. The researchers say that being able to routinely track this in the future, particularly during healthcare crises, would allow the NHS and policymakers to step in earlier to avoid a repeat of the impact of the Covid-19 pandemic.
Professor Sofat added: “Despite the incredible work done by NHS staff, our data show that we’re still not identifying people with cardiovascular risk factors at the same rate as we were before the pandemic. Detecting these risk factors early and beginning medication where appropriate is crucial to managing them, helping more people to avoid a preventable heart attack or stroke so they can live in good health for longer.”
Dr. Sonya Babu-Narayan, Associate Medical Director at the British Heart Foundation and consultant cardiologist, said: “Yet again we’re seeing clear evidence of the major disruption to healthcare people in the UK experienced during the Covid-19 pandemic. But it’s not too late to limit the damage. These findings demonstrate how getting heart healthcare back on track can curb the additional strain that untreated risk factors such as high blood pressure would otherwise place on the NHS.
She concludes, “We need to make it easier and more accessible for everyone to know their numbers – particularly their blood pressure and cholesterol. This means empowering people to access the help they need when they need it so they can be supported to manage their own health.”
Reference: “The impact of the COVID-19 pandemic on cardiovascular disease prevention and management” by Caroline E. Dale, Rohan Takhar, Raymond Carragher, Michail Katsoulis, Fatemeh Torabi, Stephen Duffield, Seamus Kent, Tanja Mueller, Amanj Kurdi, Thu Nguyen Le Anh, Stuart McTaggart, Hoda Abbasizanjani, Sam Hollings, Andrew Scourfield, Ronan A. Lyons, Rowena Griffiths, Jane Lyons, Gareth Davies, Daniel Harris, Alex Handy, Mehrdad A. Mizani, Christopher Tomlinson, Johan H. Thygesen, Mark Ashworth, Spiros Denaxas, Amitava Banerjee, Jonathan A. C. Sterne, Paul Brown, Ian Bullard, Rouven Priedon, Mamas A. Mamas, Ann Slee, Paula Lorgelly, Munir Pirmohamed, Kamlesh Khunti, Andrew D. Morris, Cathie Sudlow, Ashley Akbari, Marion Bennie, Naveed Sattar, Reecha Sofat and CVD-COVID-UK Consortium, 19 January 2023, Nature Medicine. DOI: 10.1038/s41591-022-02158-7
The British Heart Foundation Data Science Centre is part of Health Data Research UK and is funded by the British Heart Foundation.
COVID-19 infection can cause changes in calcium channels that can affect how the heart beats, it can also trigger inflammation and oxidative stress in the heart.
Potentially life-threatening heart issues can be caused by COVID-19 infections. Scientific studies suggest that people with COVID-19 are 55% more likely to suffer a major adverse cardiovascular event, including heart attack, stroke, and death, than those without COVID-19. They’re also more likely to have other heart issues, like arrhythmias (abnormal heart rhythms) and myocarditis (inflammation of the heart muscle).
Andrew Marks, a cardiologist and biophysics professor at Columbia University, Steven Reiken, a research scientist in Marks’ lab, and colleagues, have studied some of the changes that occur in the heart that could lead to these problems. Reiken will present their work on Monday, February 20 at the 67th Annual Biophysical Society Meeting in San Diego, California.
In heart tissue from patients who had COVID-19, the team observed increases in oxidative stress (harmful production of unstable molecules) and signals of inflammation, as well as changes in calcium. They also detected adverse changes to a protein called RyR2, which is responsible for regulating the heart’s calcium ion levels. The heart muscle, like all muscle cells, needs calcium ions to contract. The heart’s system for managing calcium ions is essential for the coordinated contractions of the atria and ventricles that pump blood throughout the body. When calcium in the heart becomes dysregulated, it can cause arrhythmias or heart failure.
To study changes to the heart further, they used a mouse model infected with COVID-19. They observed changes to the heart tissue including immune cell infiltration, collagen deposition (indicative of injury), death of heart cells, and blood clots. They also measured changes to the heart proteome—the proteins that are expressed by the heart cells—and found patterns consistent with changes observed to human hearts that were infected with COVID-19, as well as markers of cardiomyopathy, which can make it harder for the heart to pump blood to the body and can lead to heart failure.
“The more awareness you build around particular aspects of a disease, the more likely you are to improve the care of patients. And doctors should be aware of heart changes related to COVID-19 infections and should be looking for them,” Marks said.
Ultimately, “we want to really figure out what’s causing the heart disease and how to fix it,” Marks said. Understanding changes at the molecular level may reveal drug targets that could improve cardiac symptoms related to COVID-19 and help healthcare professionals diagnose and treat these issues more effectively. Additionally, understanding the cardiac complications of COVID-19 can also help public health officials make more informed decisions about how to respond to the COVID-19 pandemic, especially in advising those at higher risk for heart problems.
CLAIM: British telephone booths are being retrofitted with defibrillators because the COVID-19 vaccines are causing more cardiac arrests.
AP’S ASSESSMENT: False. A movement to install defibrillators in telephone kiosks across the U.K. is more than a decade old and didn’t result from the coronavirus or vaccines, according to Community Heartbeat Trust, the charity that originated the idea. One of the lifesaving devices featured in many recent posts was installed in the U.K. in 2017, years before the pandemic. Cardiologists say there’s no evidence to suggest COVID-19 vaccines are causing an increased rate of cardiac arrests.
THE FACTS: A video of a telephone booth-turned-defibrillator in the British countryside amassed millions of views on Twitter this week, alongside suggestions that it symbolized a new movement to mitigate vaccine-related deaths by installing the tool in public spaces.
The video shows one of the U.K.’s iconic red phone booths nestled beside a stone wall and in front of a stone cottage, with a yellow defibrillator visible inside.
“A British phone booth that’s been converted into a defibrillator. I wonder why the government is installing defibrillators on the streets now,” read one tweet, adding a syringe emoji to suggest the move was linked to vaccines.
“The new normal,” wrote a Twitter user that has spread numerous debunked claims about vaccines causing medical emergencies and deaths.
However, the defibrillator shown in the video is not new as the posts imply, nor is the effort to install the devices in telephone booths a result of the pandemic, according to the nonprofit that started it.
“I can categorically state that these are NOT appearing as a result of COVID,” Community Heartbeat Trust National Secretary Martin Fagan wrote in an email to The Associated Press, calling the claims “misinformation.”
A cabinet number on the device that is visible in the video reveals it is in Corfe Castle, a village in Dorset, England. It was installed in June 2017 after a fundraising campaign by the wife of a man who died cycling, Fagan wrote. The man led a specialized food company, and to raise funds, the company sold a special yogurt, Fagan said.
“In total, 17 locations were installed across the UK in his memory, at locations that meant something to him,” Fagan wrote. “It is a great story and case history.”
The device is one of around a thousand that Community Heartbeat Trust has installed in telephone booths across the U.K. in a movement that started in 2009, Fagan said. Other organizations have followed the charity’s lead, repurposing outdated telephone boxes to house the devices, which significantly improves chances of survival when used after sudden cardiac arrest.
News reports dating back a decade back up Fagan’s comments, showing telephone kiosks have long been converted into defibrillators across the U.K. and Ireland as a response to sudden cardiac arrests in the population.
Cardiologists told the AP that having the devices available in public spaces has greatly improved survival rates in people who experience a cardiac emergency.
Despite widespread online claims that COVID-19 vaccines are causing cardiac arrests, cardiologists say there’s no evidence of a link between the two, among athletes or in the general population.
“We have not seen an increase in sudden cardiac arrest as it relates to the vaccine,” said Dr. Matthew Martinez, director of sports cardiology at Atlantic Health System in Morristown Medical Center.
Monitoring systems that track people who have been vaccinated would have identified a link between the vaccine and cardiac arrest if it existed, and they haven’t, said Dr. Paul Offit, director of the Vaccine Education Center at Children’s Hospital of Philadelphia.
Studies examining rare cases of myocarditis and pericarditis—inflammation of the heart muscle or its surrounding tissues that is typically mild—after vaccination haven’t found any increased risk of death or cardiac arrest among the those who’ve received COVID-19 shots, according to the British Heart Foundation.
Smidt Heart Institute researchers show the risk of developing postural orthostatic tachycardia syndrome, or POTS, is five times higher after COVID-19 than after vaccination.
A team of investigators from the Smidt Heart Institute at Cedars-Sinai has published research in the journal Nature Cardiovascular Research that confirms a connection between Postural Orthostatic Tachycardia Syndrome (POTS) and both COVID-19 and COVID-19 vaccination.
The study suggests that a small proportion of individuals who have been vaccinated against COVID-19 may develop POTS, which is a debilitating heart condition characterized by an abnormal increase in heart rate upon standing. Furthermore, their findings indicate that people diagnosed with COVID-19 are five times more likely to develop POTS after contracting the virus than after vaccination, emphasizing the importance of receiving the vaccine.
“The main message here is that while we see a potential link between COVID-19 vaccination and POTS, preventing COVID-19 through vaccination is still the best way to reduce your risk of developing POTS,” said Alan C. Kwan, MD, first and corresponding author of the study and a cardiovascular specialist at Cedars-Sinai.
Postural orthostatic tachycardia syndrome is a nervous system-related condition that most commonly affects young women of childbearing age. The most identifiable POTS symptom is a rapid increase in the heartbeat of more than 30 beats per minute or a heart rate that exceeds 120 beats per minute, within 10 minutes of standing.
Other symptoms include fainting, dizziness, and fatigue, although some patients with severe disease may also experience migraine, increased urination, sweaty extremities, anxiety, and tremor.
To validate their findings, the study authors used data from 284,592 vaccinated patients treated within the broader Cedars-Sinai Health System between the years 2020 and 2022, as well as 12,460 Cedars-Sinai patients with COVID-19.
“From this analysis, we found that the odds of developing POTS are higher 90 days after vaccine exposure than the 90 days prior to exposure,” said Kwan. “We also found that the relative odds of POTS were higher than would be explained by increases in visits to physicians after vaccination or infection.”
Kwan emphasizes that despite this finding, the rates of POTS after vaccination were much lower than rates of new POTS diagnosis after COVID-19.
“This knowledge identifies a possible—yet still relatively slim—association between COVID-19 vaccination and POTS,” said Kwan.
Many patients—especially those who developed POTS prior to the COVID-19 pandemic—spent years trying to get properly diagnosed. This is because many healthcare providers are unfamiliar with the disease and its symptoms, which often can be incorrectly attributed to chronic fatigue syndrome or other conditions. However, COVID-19 has expanded the medical field’s understanding of POTS.
“In an unexpected but important way, the COVID-19 pandemic brought a great deal of awareness to POTS—both to patients and providers,” said Peng-Sheng Chen, MD, an expert on the condition who leads one of only a few POTS specialty clinics in the nation. “Given a broader understanding of the disease, many patients can be diagnosed more quickly permitting earlier interventions that can greatly improve their symptoms.”
Many effective interventions involve lifestyle modifications, Chen says, including avoiding triggers such as prolonged standing, extreme heat, extreme cold, and alcoholic beverages. Additional recommended measures may include eating a high-sodium diet and wearing abdominal or lower-body compression garments. Certain medical therapies can also be considered.
Patients treated for POTS at the Smidt Heart Institute often are encouraged to join the cardiac rehabilitation program, which aims to strengthen the body and heart.
While the Nature Cardiovascular Research study sheds important light on vaccinations and POTS, researchers say it has its limitations. The hope, however, is this new knowledge will help improve conversations around COVID-19 and vaccines.
“We recognize as clinicians that side effects from vaccines can vary in type and severity, even if still uncommon overall. We hope that clearer data and improved understanding will eventually enhance medical trust and quality of care as well as communications around vaccines,” said Kwan. “Ultimately, our goal is to optimize vaccine uptake.”
Reference: “Apparent risks of postural orthostatic tachycardia syndrome diagnoses after COVID-19 vaccination and SARS-Cov-2 Infection” by Alan C. Kwan, Joseph E. Ebinger, Janet Wei, Catherine N. Le, Jillian R. Oft, Rachel Zabner, Debbie Teodorescu, Patrick G. Botting, Jesse Navarrette, David Ouyang, Matthew Driver, Brian Claggett, Brittany N. Weber, Peng-Sheng Chen and Susan Cheng, 12 December 2022, Nature Cardiovascular Research. DOI: 10.1038/s44161-022-00177-8
Cedars-Sinai Medical Center
Microbiome: From Research and Innovation to Market
