Coronavirus can break your heart / Heart - related study

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Re: Coronavirus can break your heart / Heart - related study

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How does the coronavirus affect the heart?

In some people, as COVID-19 decreases lung function, it may deprive the heart of adequate oxygen.


10/29/20

https://www.king5.com/article/news/heal ... 07451057ef


How does COVID-19 affect the heart?

Even though it’s known as a respiratory virus, doctors believe the coronavirus can directly infect the heart muscle and cause other problems leading to heart damage.

In some people, as COVID-19 decreases lung function, it may deprive the heart of adequate oxygen. Sometimes it causes an overwhelming inflammatory reaction that taxes the heart as the body tries to fight off the infection.

The virus can also invade blood vessels or cause inflammation within them, leading to blood clots that can cause heart attacks.

Clots throughout the body have been found in many COVID-19 patients. That has led some doctors to try blood thinners, although there is no consensus on that treatment.

Dr. Sean Pinney of the University of Chicago says people with heart disease are most at risk for virus-related damage to the heart. But heart complications also have been found in COVID-19 patients with no known previous disease.


A recent review in the Journal of the American College of Cardiology notes that evidence of heart involvement has been found in at least 25% of hospitalized coronavirus patients. At some centers, the rate is 30% or higher. And some studies have found elevated enzyme levels and other signs suggesting heart damage even in patients with milder disease. It is not known whether that damage is permanent.

One small study found evidence of the virus in the hearts of COVID-19 patients who died from pneumonia. Another, using heart imaging, found inflammation of the heart muscle in four college athletes who had recovered from mild COVID-19 infections. There were no images available from before the athletes got sick, and therefore no way to know if they had pre-existing heart problems.

Dr. Tom Maddox, an American College of Cardiology board member, says it's unclear if the virus can cause a normal heart to become dysfunctional.

“There’s still so much we don’t know," Maddox said.

The United States has more than 8.8 million confirmed cases of COVID-19, according to data from Johns Hopkins University.

As of Wednesday, the U.S. had more than 227,000 deaths from the virus. Worldwide, there are more than 44 million confirmed cases with more than 1.1 million deaths.
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Re: Coronavirus can break your heart / Heart - related study

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Study shows SARS-CoV-2 direct heart muscle cell infection, cell death, loss of contractility

11/8/20


https://www.news-medical.net/news/20201 ... ility.aspx


The coronavirus disease (COVID-19) is a respiratory illness that affects the lungs. The most common symptoms associated with the infection include fever, a continuous dry cough, and difficulty breathing (dyspnea or shortness of breath). In more severe cases, the illness causes viral pneumonia. In more critical cases, it can eventually lead to acute respiratory distress syndrome (ARDS), which can often be fatal.

As the COVID-19 pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) agent, has evolved, more evidence is coming to light that the virus can also affect other organs in the body, including the heart and brain.

An illuminating new study conducted by researchers at the Washington University School of Medicine, the University of Wisconsin Hospital, Baylor College of Medicine, Vanderbilt University, Creighton University the University of Texas Medical Branch, The Jackson Laboratory for Genomic Medicine, USA and the University of Heidelberg, Germany, shows that SARS-CoV-2 can infect heart cells in a lab dish (in vitro), indicating it may be possible for heart cells in COVID-19 patients to be directly infected by the virus.

The study

Recent studies on COVID-19 have shown evidence of cardiac involvement, showing that myocardial injury and myocarditis are predictors of poor outcomes in severely ill patients. Nevertheless, little is known regarding SARS-CoV-2 tropism within the heart and whether cardiac complications stem from myocardial infection.

To arrive at the study’s findings, the researchers developed a human-engineered heart tissue (EHT) model. They tested the hypothesis that SARS-CoV-2 induces heart pathology by infecting heart cells and activating immune responses.

Study findings

The team showed that the virus selectively infects and replicates within hPSC-derived cardiomyocytes, resulting in cell death. Based on the study’s findings, the team noted that cardiomyocyte or heart cell infection is dependent on the angiotensin-converting enzyme 2 (ACE2) expression and endosomal cysteine protease activity.

In the study, which appeared on the preprint bioRxiv* server, the researchers revealed that SARS-CoV-2-infected EHTs manifested the typical characteristics of myocarditis or heart inflammation. These include the stimulation of immune cells, heart cell death, and decreased contractile force generation.

The team also noted that the autopsy and biopsy samples from four patients who tested positive for COVID-19 and myocarditis exhibited patchy cardiomyocyte infection, along with myocardial cell death and the accumulation of macrophages, which are specialized cells involved in the detection, phagocytosis, and destruction of bacteria and other harmful organisms.

The team also explored if human heart cells may be susceptible to SARS-CoV-2 infection. They studied the expression of the angiotensin-converting enzyme 2 (ACE2) within the human heart. Past studies have shown that ACE2 acts as a cell-surface receptor for SARS-CoV-2 and binds with the virus spike protein (sometimes referred to as its S-protein) in many human cell types. The team unveiled that cardiomyocytes express ACE2 and they showed a significant variation in ACE2 expression between cardiomyocytes.

“We provide evidence that SARS-CoV-2 readily infects and replicates within human cardiomyocytes, indicating that viral infection likely contributes to the pathogenesis of COVID-19 myocarditis,” the team explained.

The team believes that engineered heart tissue has paved the way to gain better insights into the link between heart cell infection, myocardial inflammation, and contractile dysfunction. Also, EHTS can help scientists determine the various effects of COVID-19 on the human heart, helping clinicians provide better interventions and reduce mortality among patients.

“We provide evidence that human EHTs recapitulate many features of COVID-19 myocarditis, demonstrate that SARS-CoV-2 infection of EHTs can produce multiscale changes spanning from the molecular to functional levels, and show that EHTs serve as useful tools for dissecting mechanisms that contribute to cardiac pathology,” the team concluded.

The coronavirus pandemic continues to ravage across the globe. Overall, there are over 50 million confirmed cases, and at least 1.25 million deaths. The United States remains the country with the highest number of cases, reaching 9.96 million. India and Brazil follow with a staggering 8.5 million and 5.66 million cases, respectively.

*Important Notice

bioRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.

Source:

COVID-19 Dashboard by the Center for Systems Science and Engineering (CSSE) at Johns Hopkins University (JHU) - https://gisanddata.maps.arcgis.com/apps ... 7b48e9ecf6

Journal reference:

Penna, V., Lai, L., Winkler, E., Sviben, S., et al. (2020). SARS-CoV-2 Infects Human Engineered Heart Tissues and Models COVID-19 Myocarditis. bioRxiv. https://www.biorxiv.org/content/10.1101 ... 4.364315v1
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Re: Coronavirus can break your heart / Heart - related study

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Study investigates link between myocarditis and COVID-19

11/19/20


https://www.news-medical.net/news/20201 ... ID-19.aspx


As the COVID-19 pandemic evolves, so too does research into its effects on heart health. One particular area of interest for physicians involves whether COVID-19 leads to inflammation of the heart muscle, a condition known as myocarditis.

According to the Myocarditis Foundation, myocarditis most often affects young, healthy and athletic people. Those at highest risk are people from puberty through their early 30s. Myocarditis affects men twice as often as women. If left untreated, it can lead to heart failure. It's also a cause of sudden cardiac death.

As researchers monitored COVID-19 patients and looked for evidence of myocarditis, they found a significant number of people with severe COVID-19 cases who had heart trouble.

It usually took the form of the heart not working well and developing the clinical symptoms of heart failure, but doing so in the setting of severe, systemic illness."

But what remained unclear is whether myocarditis and other heart failure-related symptoms were caused specifically by COVID-19 or other health conditions.

Early research appeared to indicate a direct link. A study conducted in Frankfurt, Germany, reported the results of cardiac magnetic resonance imaging (MRI) tests on a cohort of 100 patients recently recovered from COVID-19. The results, published in July 2020, revealed ongoing heart inflammation in 60% of patients and cardiac involvement in 78% of patients. "But ongoing studies have failed to replicate those results," Boehmer said.

A smaller study, published in September 2020, examined cardiac MRI results from 26 college athletes at The Ohio State University who had COVID-19 symptoms. The results showed that 15% of those athletes appeared to have myocarditis.

" These findings led many athletic programs-;including those associated with Big 10 Conference schools such as Penn State-;to enact aggressive screening programs for student athletes. "So far, we're not finding myocarditis or significant heart involvement with cardiovascular disease in patients with limited symptoms," Boehmer said. "It doesn't seem that exercise and cardiovascular outcomes are correlated with the pandemic, which is a very reassuring observation."

- Dr John Boehmer, Cardiologist, Penn State Heart and Vascular Institute

A special communication written by a team of sports cardiologists and published in JAMA Cardiology in October 2020 supports Boehmer's observations. It states: "Our combined experience suggests that most athletes with COVID-19 are asymptomatic to mildly ill, and to date, return-to-play risk stratification has yielded few cases of relevant cardiac pathology."

While more research is needed to fully determine a connection between myocarditis and COVID-19, anyone involved in any type of athletic activity should take precautions before returning to work or play. The JAMA Cardiology communication recommends athletes slowly increase their activity after recovering from asymptomatic or mild cases of COVID-19.

People with moderate-to-severe COVID-19 should convalesce for two weeks after symptoms clear, and then should slowly resume physical activity under the guidance of their health care provider and athletic training team.

Although Boehmer hasn't seen an increase in myocarditis or related symptoms in COVID-19 patients locally during the pandemic, he has seen one troubling trend. "There's an excess of heart and vascular death due to people putting off regular medical care because they're afraid to come to the hospital," he said.

People should watch for the signs of emergency heart problems-;chest pain, jaw or neck pain, discomfort in the arms and shoulders, shortness of breath-;and call 911 if they suspect a heart attack. "We've taken all precautions to keep patients safe at Penn State Health Milton S. Hershey Medical Center," Boehmer said. "Following up with a doctor and getting all the testing you need for any heart condition are the best things you can do for your heart."
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Re: Coronavirus can break your heart / Heart - related study

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Indirect effects of COVID-19 pandemic on cardiovascular disease patients and care

1/11/21


https://www.news-medical.net/news/20210 ... -care.aspx


Deaths from ischemic heart disease and hypertensive diseases in the United States increased during the COVID-19 pandemic over the prior year, while globally, COVID-19 was associated with significant disruptions in cardiovascular disease testing. These findings are from two papers publishing in the Journal of the American College of Cardiology that examined the indirect effects of the pandemic on cardiovascular disease patients and their care.

The impact of the COVID-19 pandemic has been substantial, but there are concerns about the indirect impact of the pandemic as well, particularly for heart disease patients. Many reports have suggested that large mortality increases during the pandemic cannot be explained by COVID-19 alone. During the height of stay-at-home orders in the U.S., hospitals reported a decline in the number of heart attack and stroke patients being diagnosed and treated at the hospital. The assumption was that some patients feared contracting COVID-19 at a hospital and were choosing to delay care or not seek care at all for emergencies, including heart attacks. The American College of Cardiology issued a statement and infographic on the safety of hospitals during the COVID-19 pandemic and urged people to seek immediate care if needed.
Cardiovascular deaths during the COVID-19 pandemic in the United States

In this study, researchers examined whether population-level deaths due to cardiovascular causes (ischemic heart disease, heart failure, hypertensive diseases, cerebrovascular disease and other disease of circulatory system) changed in the U.S. during the early phase of the pandemic, relative to the same period in the year prior, and if these changes were more pronounced in states that experienced the initial surge of COVID-19 cases.

Using data from the National Center for Health Statistics, researchers looked at death rates from cardiovascular causes in the U.S. from March 18, 2020 - June 2, 2020 (the pandemic) and January 1, 2020 - March 17, 2020 (before the pandemic) and compared them to the same periods in 2019. They found that deaths from ischemic heart disease and hypertensive diseases increased after the onset of the pandemic in 2020, compared with changes over the same period in 2019. In contrast, deaths caused by heart failure, cerebrovascular disease or other diseases of the circulatory system did not change nationally. New York City experienced the largest relative increase in deaths due to ischemic heart disease (139%) and hypertensive diseases (164%) during the pandemic. The remainder of New York state, New Jersey, Michigan and Illinois also experienced significant increases in deaths due to these conditions, while Massachusetts and Louisiana did not see a change in cardiovascular deaths.

"Our findings suggest that the pandemic may have had an indirect toll on patients with
cardiovascular disease, potentially due to the avoidance of hospitals out of fear of exposure to the virus, increased health care system strain and the deferral of semi-elective procedures and care," said Rishi K. Wadhera, MD, MPP, MPhil, lead author of the study, a cardiologist at Beth Israel Deaconess Medical Center and an assistant professor at Harvard Medical School. "U.S. public health officials and policymakers should improve public health messaging to encourage patients with acute conditions to seek medical care."

International impact of COVID-19 on the diagnosis of heart disease

The COVID-19 pandemic caused health care delivery disruptions across the globe in 2020, including delays in cardiovascular disease diagnosis and timely treatment. Heart disease is the No. 1 killer worldwide, and outcomes are dependent on early and effective diagnosis to determine the best possible treatment. In this study researchers sought to determine the full magnitude of reductions in diagnostic heart disease procedures in 2020 and how that might impact long-term cardiovascular disease outcomes.

Surveys were submitted from 909 inpatient and outpatient centers performing cardiac
diagnostic procedures in 108 countries. According to researchers, procedure volumes decreased 42% from March 2019 to March 2020, and 64% from March 2019 to April 2020. Specifically, transthoracic echocardiography decreased by 59%, transesophageal echocardiography by 76% and stress tests by 78%. Coronary angiography (invasive or computed tomography) decreased 55%. Researchers also classified countries into four economic levels (low, lower-middle, upper-middle and high) and found that location in a low/lower-middle income country was associated with an additional 22% reduction in cardiac procedures and less availability of personal protective equipment and telehealth.


" These findings raise serious concerns for long-term adverse cardiovascular health outcomes resulting from decreased diagnosis. Efforts to improve timely patient access to cardiovascular diagnosis in this and future pandemics, particularly in low- and middle-income countries, are warranted."

- Andrew J. Einstein, MD, PhD, Associate Professor of Medicine, Columbia University Vagelos College of Physicians and Surgeons, and Cardiologist, New York-Presbyterian/Columbia University Irving Medical Center

Source:


American College of Cardiology
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Re: Coronavirus can break your heart / Heart - related study

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Patient with hypertension or cardiovascular diseases experienced critical disease progression with COVID-19

1/11/21


https://www.news-medical.net/news/20210 ... ID-19.aspx


COVID-19 patients who also suffer from high blood pressure are more likely to fall severely ill with the disease, which also leaves them at greater risk of death.

Scientists from the Berlin Institute of Health (BIH) and Charité – Universitätsmedizin Berlin, in collaboration with partners in Heidelberg and Leipzig, have now found that the immune cells of patients with hypertension are already pre-activated and that this pre-activation is greatly enhanced under COVID-19.

This most likely explains the augmented response of the immune system and the more severe disease progression. However, certain hypertension-reducing drugs known as ACE inhibitors can have a beneficial effect.

They not only lower blood pressure but also counteract immune hyperactivation. The scientists have now published their findings in the journal Nature Biotechnology.

More than one billion people worldwide suffer from high blood pressure or hypertension. Of the more than 75 million people around the world who have become infected with the SARS-CoV-2 virus worldwide so far, more than 16 million also have hypertension.

These patients are more likely to become severely ill, which in turn results in an increased risk of death. It was previously unclear to what extent treatment with antihypertensive drugs could be continued during a SARS-CoV-2 infection - and whether they were more likely to benefit or harm the patients.

This is because antihypertensives interfere with the exact same regulatory mechanism that the novel coronavirus SARS-CoV-2 uses to enter the host cell and trigger COVID-19.

Professor Ulf Landmesser is Medical Director of the CharitéCenter 11 for Cardiovascular Diseases, Director of the Medical Department of Cardiology, and BIH Professor of Cardiology on the Charité's Campus Benjamin Franklin in Berlin. He recognized early on that patient with hypertension or cardiovascular diseases often experienced a particularly critical disease progression with COVID-19.

" The virus uses the receptor ACE2 as an entry portal into the cells, and the formation of this receptor is potentially influenced by the administration of antihypertensive drugs. We had therefore initially feared that patients receiving ACE inhibitors or angiotensin receptor blockers might have more ACE2 receptors on their cell surfaces and thus become more easily infected."

- Ulf Landmesser, Professor, Medical Director of the CharitéCenter, Director of the Medical Department of Cardiology, BIH at Charité

Certain drugs that lower blood pressure could also help with COVID-19

To clarify this suspicion, the scientists analyzed individual cells from the respiratory systems of COVID-19 patients who were also taking medication for high blood pressure.

Dr. Sören Lukassen, a scientist in Professor Christian Conrad's group at the BIH Digital Health Center, explains that they were subsequently able to give the all-clear: "We found that the drugs do not seem to cause more receptors to form on the cells. As a result, we do not believe that they make it easier for the virus to enter the cells in this way and thus cause the more severe course of COVID-19."

On the contrary, cardiovascular patients taking ACE inhibitors actually displayed a lower risk of becoming severely ill with COVID-19. In fact, they displayed almost the same level of risk as COVID-19 patients without cardiovascular problems.

Severe course of COVID-19 linked to pre-activation of the immune system

The blood of hypertensive patients usually shows elevated levels of inflammation, which can be fatal in the case of a SARS-CoV-2 infection. "Elevated inflammation levels are always a warning signal that COVID-19 will be more severe, regardless of any cardiovascular issues," explains Landmesser.

The scientists, therefore, employed single-cell sequencing methods to investigate the immune response of hypertensive patients with COVID-19.

"We analyzed a total of 114,761 cells from the nasopharynx of 32 COVID-19 patients and 16 non-infected controls, with both groups including cardiovascular patients as well as people without cardiovascular problems," reports Dr. Saskia Trump, research group leader in the lab of Irina Lehmann, who is BIH Professor for Environmental Epigenetics and Lung Research.

"We found that the immune cells of the cardiovascular patients displayed strong pre-activation even before infection with the novel coronavirus," explains Lehmann.

"After contact with the virus, these patients were more likely to develop an augmented immune response, which was associated with the severe disease progression of COVID-19. However, our results also showed that treatment with ACE inhibitors, though not with angiotensin receptor blockers, could prevent this augmented immune response following infection by the coronavirus. ACE inhibitors could thus reduce the risk of patients with hypertension from experiencing severe disease progression."

Delayed reduction in viral load

Furthermore, the scientists found that the anti-hypertensive drugs can also impact how quickly the immune system is able to reduce the viral load, i.e., the concentration of the virus in the body. "Here, we observed a clear difference between the different forms of treatment for high blood pressure," notes Roland Eils, Director of the BIH Digital Health Center.

"In the patients treated with angiotensin II receptor blockers, the reduction in viral load was significantly delayed, which could also contribute to a more severe course of COVID-19. We did not observe this delay in the patients who were receiving ACE inhibitors to treat their hypertension."
Interdisciplinary collaboration speeds up research

More than 40 scientists have been working at a breakneck pace on this extensive study. "The ability to quickly provide answers to urgent questions during the ongoing pandemic requires interdisciplinary collaboration among many committed individuals," explains Eils.

"COVID-19 is such a complex disease that we brought together experts from cardiology, immunology, virology, pulmonary medicine, intensive care and computer science for this study. Our goal was to provide a scientifically sound answer as quickly as possible to the question of whether simultaneous treatment with ACE inhibitors or angiotensin receptor blockers could have beneficial or even adverse effects during the COVID-19 pandemic."

No evidence of increased risk of infection

Thanks to the study, the teams from the BIH, Charité, and collaborating institutions in Leipzig and Heidelberg can now reassure both patients and the physicians treating them: "Our study provides no evidence that treatment with anti-hypertensive drugs increases the risk of infection by the novel coronavirus," says Ulf Landmesser, summarizing the results.

"However, treating hypertension with ACE inhibitors could be more beneficial for patients suffering from COVID-19 than treatment with angiotensin II receptor blockers - a hypothesis that is currently being further investigated in randomized trials."

Source:

BIH at Charité

Journal reference:

Trump, S., et al. (2020) Hypertension delays viral clearance and exacerbates airway hyperinflammation in patients with COVID-19. Naure Biotechnology. doi.org/10.1038/s41587-020-00796-1.
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Re: Coronavirus can break your heart / Heart - related study

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COVID-19 will impact cardiovascular disease deaths for years to come, warn experts

1/27/21

https://www.news-medical.net/news/20210 ... perts.aspx


Heart disease remains the leading cause of death worldwide, according to the American Heart Association's Heart Disease and Stroke Statistics -- 2021 Update, published today in the Association's flagship journal Circulation, and experts warn that the broad influence of the COVID-19 pandemic will likely continue to extend that ranking for years to come.

Globally, nearly 18.6 million people died of cardiovascular disease in 2019, the latest year for which worldwide statistics are calculated. That reflects a 17.1% increase over the past decade. There were more than 523.2 million cases of cardiovascular disease in 2019, an increase of 26.6% compared with 2010.

Experts predict the global burden of cardiovascular disease will grow exponentially over the next few years as the long-term effects of the current COVID-19 pandemic evolve.

"COVID-19 has taken a huge toll on human life worldwide and is on track to become one of the top three to five causes of death in 2020. But its influence will directly and indirectly impact rates of cardiovascular disease prevalence and deaths for years to come," said Salim S. Virani, M.D., Ph.D., FAHA, chair of the writing committee for the 2021 Statistical Update and an associate professor in cardiology and cardiovascular research sections at Baylor College of Medicine in Houston, Texas. "Research is showing that the unique coronavirus can cause damage to the heart. Importantly, we also know people have delayed getting care for heart attacks and strokes, which can result in poorer outcomes."

But Virani said an even more critical issue will be the cardiovascular health risks that are exacerbated by the poor lifestyle behaviors that have been prevalent throughout the pandemic.

" The extraordinary circumstances of dealing with COVID-19 have changed the way we live, including adopting unhealthy behaviors that are known to increase the risk of heart disease and stroke. Unhealthy eating habits, increased consumption of alcohol, lack of physical activity and the mental toll of quarantine isolation and even fear of contracting the virus all can adversely impact a person's risk for cardiovascular health. We'll need to watch and address these trends as the full ramifications will likely be felt for many years to come."

- Salim S. Virani, M.D., Ph.D., FAHA, Associate Professor in Cardiology and Cardiovascular Research Sections, Baylor College of Medicine in Houston, Texas

Based on the 2021 Statistical Update, which furnished U.S. mortality data from 2018, cardiovascular disease remains the leading cause of death in the U.S. In the year 2020, approximately 360,000 lives were lost to COVID-19 in the U.S.; the release of data regarding all causes of death in the coming years will enable rank comparison of disease-specific causes of mortality that include COVID-19.

Tracking such trends is one of the reasons the American Heart Association publishes the definitive statistical update annually, providing a comprehensive resource of the most current data, relevant scientific findings and assessment of the impact of cardiovascular disease nationally and globally.

The annual update represents a compilation of the newest, most relevant statistics on heart disease, stroke and risk factors impacting cardiovascular health.

The U.S. data is gathered in conjunction with the National Institutes of Health and other government agencies, while the global trends are provided by the Global Burden of Disease Study from the Institute for Health Metrics and Evaluation at the University of Washington.

New in this year's report is a chapter devoted to adverse pregnancy outcomes, which are known to increase the risk of cardiovascular disease in mothers and their babies. Pregnancy complications including hypertensive disorders, gestational diabetes, preterm births and small for gestational age at birth deliveries occur in 10% to 20% of all pregnancies in the U.S. Cardiovascular deaths are the most common cause (26.5%) of maternal death in the U.S.

"We must address this issue to save the lives of mothers and to improve the health of their children at birth, but also over their lifetime," Virani said. "There can be long-term effects on offspring of women who suffer pregnancy-related complications. But we can also help impact the health of future generations because as we help women learn to reduce their cardiovascular risk, they're likely to adopt healthier lifestyles. In turn, they can influence the health behaviors of their families."

The annual report continues to track trends related to ideal cardiovascular health, social determinants of health, global cardiovascular health, cardiovascular health genetics and health care costs. Virani emphasized the importance of this surveillance as a critical resource for the lay public, policy makers, media professionals, clinicians, health care administrators, researchers, health advocates and others seeking the best available data on these factors and conditions.

This statistical update was prepared by a volunteer writing group on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee.

Source:

American Heart Association

Journal reference:


Virani, S. S., et al. (2021) Heart Disease and Stroke Statistics—2021 Update: A Report From the American Heart Association. Circulation. doi.org/10.1161/CIR.0000000000000950.
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Re: Coronavirus can break your heart / Heart - related study

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Mortality from sudden cardiac arrest is higher in COVID-19 patients

2/6/21


https://www.news-medical.net/news/20210 ... ients.aspx


Sudden cardiac arrest is more often fatal in people with COVID-19, a new study shows. Those responsible for the research see the results as a wake-up call for the public and care providers alike.

The survey now published in the European Heart Journal is a register-based observation study. It covers all 3,026 cases of sudden cardiac arrest that were reported to the Swedish Registry for Cardiopulmonary Resuscitation in the period from 1 January to 20 July 2020 -- that is, both before and during the pandemic.

The Registry's statistics show that, in Sweden, there are 6,000 cases of sudden cardiac arrest annually in which the person is not admitted to hospital. Some 600 of these people survive. The corresponding figures for cardiac arrest during inpatient care are 2,500 cases and 900 survivors.

The study results indicate that mortality from sudden cardiac arrest is higher if the person has COVID-19, but that different patient groups show divergent differences in mortality rates.

During the study period, 1,946 cases of sudden cardiac arrest outside of hospitals were registered. In 10 percent of the cases in this group, the person had COVID-19, and the risk of a fatal outcome proved to be 3.4 times higher for these people than for the other group members.

Of the 1,080 cases of sudden cardiac arrest that took place in hospitals, COVID-19 was present in 16 percent. Among the patients with COVID-19, mortality was 2.3 times higher than for the others in this group.

The largest mortality difference was noted in the group of women who were already receiving inpatient care at the time of their cardiac arrest. In these women, ongoing COVID-19 infection was associated with nine times the risk of a fatal outcome during the initial months and a sevenfold risk from April onward.

The study, carried out by researchers at the Swedish Registry for Cardiopulmonary Resuscitation and the University of Gothenburg, received financial support from the Swedish Heart-Lung Foundation. This Foundation's prompt funding action was crucial for the implementation, emphasizes Araz Rawshani, registrar and researcher at the Faculty of Medicine, Sahlgrenska Academy, who also works at Sahlgrenska University Hospital.

" We hope our results can help to raise awareness of COVID-19 complications among the public, care providers, and decision-makers. That could improve care and mobilize resources for high-risk patients."

- Araz Rawshani, Researcher, Faculty of Medicine, Sahlgrenska Academy

Kristina Sparreljung is the Secretary-General of the Swedish Heart-Lung Foundation.

"We hope these results will help to enable more lives to be saved. This study is a direct result of the emergency grant provided by the Heart-Lung Foundation for research on COVID-19 connected with cardiopulmonary disease back in spring 2020," she says.

The survival rate for cardiac arrest has risen successively in recent years, but mortality remains high. Surviving a sudden cardiac arrest outside of hospital requires, pending arrival of an ambulance, immediate action in the form of cardiopulmonary resuscitation (CPR) and use of an automated external defibrillator (AED).

Source:

University of Gothenburg

Journal reference:


Sultanian, P., et al. (2021) Cardiac arrest in COVID-19: characteristics and outcomes of in- and out-of-hospital cardiac arrest. A report from the Swedish Registry for Cardiopulmonary Resuscitation. European Heart Journal. doi.org/10.1093/eurheartj/ehaa1067.
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Re: Coronavirus can break your heart / Heart - related study

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COVID-19 disrupts heart muscle contraction, may lead to heart failure

3/3/21


https://www.news-medical.net/news/20210 ... ilure.aspx


Since early in the pandemic, COVID-19 has been associated with heart problems, including reduced ability to pump blood and abnormal heart rhythms.

But it's been an open question whether these problems are caused by the virus infecting the heart, or an inflammatory response to viral infection elsewhere in the body. Such details have implications for understanding how best to treat coronavirus infections that affect the heart.

A new study from Washington University School of Medicine in St. Louis provides evidence that COVID-19 patients' heart damage is caused by the virus invading and replicating inside heart muscle cells, leading to cell death and interfering with heart muscle contraction.

The researchers used stem cells to engineer heart tissue that models the human infection and could help in studying the disease and developing possible therapies.

The study is published Feb. 26 in the Journal of the American College of Cardiology: Basic to Translational Science.

"Early on in the pandemic, we had evidence that this coronavirus can cause heart failure or cardiac injury in generally healthy people, which was alarming to the cardiology community," said senior author Kory J. Lavine, MD, Ph.D., an associate professor of medicine. "Even some college athletes who had been cleared to go back to competitive athletics after COVID-19 infection later showed scarring in the heart. There has been debate over whether this is due to direct infection of the heart or due to a systemic inflammatory response that occurs because of the lung infection.

"Our study is unique because it definitively shows that, in patients with COVID-19 who developed heart failure, the virus infects the heart, specifically heart muscle cells."

Lavine and his colleagues -; including collaborators Michael S. Diamond, MD, Ph.D., the Herbert S. Gasser Professor of Medicine, and Michael J. Greenberg, PhD, an assistant professor of biochemistry and molecular biophysics -; also used stem cells to engineer tissue that models how human heart tissue contracts. Studying these heart tissue models, they determined that viral infection not only kills heart muscle cells but destroys the muscle fiber units responsible for heart muscle contraction.

They also showed that this cell death and loss of heart muscle fibers can happen even in the absence of inflammation.

"Inflammation can be a second hit on top of the damage caused by the virus, but the inflammation itself is not the initial cause of the heart injury," Lavine said.

Other viral infections have long been associated with heart damage, but Lavine said SARS-CoV-2, the virus that causes COVID-19, is unique in the effect it has on the heart, especially in the immune cells that respond to the infection. In COVID-19, immune cells called macrophages, monocytes and dendritic cells dominate the immune response. For most other viruses that affect the heart, the immune system's T cells and B cells are on the scene.

"COVID-19 is causing a different immune response in the heart compared with other viruses, and we don't know what that means yet," Lavine said. "In general, the immune cells seen responding to other viruses tend to be associated with a relatively short disease that resolves with supportive care. But the immune cells we see in COVID-19 heart patients tend to be associated with a chronic condition that can have long-term consequences. These are associations, so we will need more research to understand what is happening."

Part of the reason these questions of causation in heart damage have been hard to answer is the difficulty in studying heart tissue from COVID-19 patients. The researchers were able to validate their findings by studying tissue from four COVID-19 patients who had heart injury associated with the infection, but more research is needed.

To that end, Lavine and Diamond, are working to develop a mouse model of the heart injury. To emphasize the urgency of the work, Lavine pointed to the insidious nature of the heart damage COVID-19 can cause.

" Even young people who had very mild symptoms can develop heart problems later on that limit their exercise capacity. We want to understand what's happening so we can prevent it or treat it. In the meantime, we want everyone to take this virus seriously and do their best to take precautions and stop the spread, so we don't have an even larger epidemic of preventable heart disease in the future."

- Kory J. Lavine, MD, PhD, Study Senior Author and Associate Professor of Medicine, Washington University School of Medicine

Source:


Washington University School of Medicine

Journal reference:

Bailey, A. L., et al. (2021) SARS-CoV-2 Infects Human Engineered Heart Tissues and Models COVID-19 Myocarditis. JACC: Basic to Translational Science. doi.org/10.1016/j.jacbts.2021.01.002.
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Re: Coronavirus can break your heart / Heart - related study

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Inflammatory heart disease is rare among professional athletes with mild COVID-19, study finds

3/4/21


https://www.news-medical.net/news/20210 ... finds.aspx


Inflammatory heart disease is a rare finding among professional athletes with mild or asymptomatic COVID-19 infection, a large-scale study has found.

The study, led by Columbia University Vagelos College of Physicians and Surgeons in collaboration with the major North American sports leagues and their respective players' associations, was published online today in JAMA Cardiology.

Athletes and COVID-19

Studies suggest that approximately 20% of patients hospitalized with severe COVID-19 develop some type of heart damage, but the impact of mild or asymptomatic infections on the heart is not known.

Viral infections can cause inflammatory heart disease--inflammation in the heart muscle (myocarditis) or the lining of the heart (pericarditis). The condition can trigger abnormal heart rhythms and accounts for approximately 5% of cases of sudden cardiac death in athletes.


" Athletes have a unique risk because of demands on the heart from strenuous exercise, which can increase the risk of abnormal heart rhythms in those with underlying inflammatory heart disease."

- David Engel, MD, Associate Professor of Medicine, Columbia University Vagelos College of Physicians and Surgeons and Senior Author

Early in the COVID-19 pandemic, isolated reports of college and professional athletes who developed heart inflammation were widely publicized, causing alarm among medical professionals, sports leagues, and universities.

In the spring of 2020, the American College of Cardiology (ACC) Sports and Exercise Cardiology section recommended that competitive athletes who test positive for SARS-CoV-2 undergo screening for inflammatory heart disease before returning to the field, court, or ice. The recommendations called for a specific screening protocol with blood tests, electrocardiography, and echocardiography. The guidelines were adopted and implemented across all of the major sports leagues, including Major League Baseball, Major League Soccer, the National Football League, the National Hockey League, and men's and women's National Basketball Associations.

"While all of the major professional leagues had implemented COVID-19 testing programs and the ACC screening protocol, there was no data on how prevalent heart inflammation may be among athletes who tested positive for the coronavirus or how effective the screening program would be to allow athletes to safely return to sport after COVID-19," Engel says. "The leagues realized that if they pooled their screening data, we would soon have an answer."

Very low incidence of heart inflammation in athletes with mild COVID-19


The study included data from 789 professional athletes across the professional leagues who were screened for post-COVID-19 cardiac inflammation. None had severe COVID-19 symptoms, and approximately 40% had very mild or no symptoms.

Abnormal cardiac screening results raising concern for potential COVID-19-associated cardiac injury were found in 30 (3.8%) of the athletes. Further assessment with diagnostic cardiac MRI and cardiac stress tests ultimately found heart inflammation in only five of the athletes (0.6%).

None of the athletes with inflammatory heart disease had a history of heart disease and all were restricted from athletic activities, in accordance with ACC guidelines.

"Our study shows that it is rare for professional athletes with mild COVID-19 to develop heart inflammation, but the risk is not zero," says Engel. "These findings give college and other athletic organizations some clinically relevant context to help them optimize their return-to-play screening protocols with a measure of confidence."

Source:

Columbia University Irving Medical Center

Journal reference:

Martinez, M.W., et al. (2021) Prevalence of Inflammatory Heart Disease Among Professional Athletes With Prior COVID-19 Infection Who Received Systematic Return-to-Play Cardiac Screening. JAMA Cardiology. doi.org/10.1001/jamacardio.2021.0565.
trader32176
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Re: Coronavirus can break your heart / Heart - related study

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COVID-19 and its impact on the cardiovascular system

3/15/21


https://openheart.bmj.com/content/8/1/e001472


Abstract

Objectives The clinical impact of SARS-CoV-2 has varied across countries with varying cardiovascular manifestations. We review the cardiac presentations, in-hospital outcomes and development of cardiovascular complications in the initial cohort of SARS-CoV-2 positive patients at Imperial College Healthcare National Health Service Trust, UK.

Methods We retrospectively analysed 498 COVID-19 positive adult admissions to our institute from 7 March to 7 April 2020. Patient data were collected for baseline demographics, comorbidities and in-hospital outcomes, especially relating to cardiovascular intervention.

Results
Mean age was 67.4±16.1 years and 62.2% (n=310) were male. 64.1% (n=319) of our cohort had underlying cardiovascular disease (CVD) with 53.4% (n=266) having hypertension. 43.2%(n=215) developed acute myocardial injury. Mortality was significantly increased in those patients with myocardial injury (47.4% vs 18.4%, p<0.001). Only four COVID-19 patients had invasive coronary angiography, two underwent percutaneous coronary intervention and one required a permanent pacemaker implantation. 7.0% (n=35) of patients had an inpatient echocardiogram. Acute myocardial injury (OR 2.39, 95% CI 1.31 to 4.40, p=0.005) and history of hypertension (OR 1.88, 95% CI 1.01 to 3.55, p=0.049) approximately doubled the odds of in-hospital mortality in patients admitted with COVID-19 after other variables had been controlled for.

Conclusion Hypertension, pre-existing CVD and acute myocardial injury were associated with increased in-hospital mortality in our cohort of COVID-19 patients. However, only a low number of patients required invasive cardiac intervention.

Key questions

What is already known about this subject?

Initial data from China and the USA suggest involvement of cardiovascular comorbidities and myocardial injury being related to death in COVID-19 patients.

What does this study add?


We aim to provide comprehensive data about COVID-19 and its cardiovascular impact on cardiovascular system in UK population. We aim to provide a detailed analysis of the impact of cardiovascular comorbidities in COVID-19 patients and the impact of myocardial injury. We also have provided a detailed analysis of cardiac intervention in this cohort of patients.

How might this impact on clinical practice?

By identifying factors associated with increased mortality, we aim to risk stratify these patients. Also by identifying patients with myocardial injury, these patients may warrant increased cardiac team involvement. Furthermore, it aims to provide an insight into managing COVID-19 patients with cardiac issues in UK population.

Introduction

SARS-CoV-2 virus was first reported in Wuhan, China, in December 2019. It has since rapidly spread throughout the world and was declared a pandemic by WHO on 11 March 2020.1 There have been more than 17 million cases reported worldwide with 675 000 deaths as of 30 July 2020. The UK has had over 300 000 patients infected and more than 41 000 deaths as of 30 July 2020.

Our understanding of COVID-19 remains limited, as the spread of the SARS-CoV-2 has been extremely rapid. Emerging data suggest that elderly patients and those with comorbidities have adverse prognosis, but the nature of the relationship between underlying cardiovascular disease (CVD), acute myocardial injury and COVID-19 outcomes remains unclear.2 Data from China suggest that acute myocardial injury in COVID-19 patients is associated with increased mortality.3 4 Infected patients have been reported to present with a wide range of cardiac issues from arrhythmias to ST elevation myocardial infarction (STEMI) mimics, excessive thrombus formation and fulminant myocarditis.5

This study describes a single centre experience of hospitalised COVID-19 patients from Imperial College Healthcare National Health Service (NHS) Trust, London, UK which comprises two receiving hospitals and one tertiary referral centre at the epicentre of the COVID-19 outbreak in the UK. We focus on the role of underlying cardiac disease and acute cardiac outcomes in these patients.

Methods

Study design


We retrospectively analysed 498 consecutive patients with confirmed SARS-CoV-2 admitted to three central London hospitals forming Imperial College Healthcare NHS Trust, London, UK from 7 March 2020 to 7 April 2020. The trust is a cardiac tertiary referral centre for West London.

Patients with possible COVID-19 symptoms, who were sufficiently unwell to require admission to hospital were included if they had an initial positive nasopharyngeal swab by viral SARS-CoV-2 reverse transcription-PCR, or if they had a high pretest probability of COVID-19 and were confirmed positive on subsequent nasopharyngeal swab. Patients with high pretest probability of COVID-19 but without positive swabs were not included. Patients who became SARS-CoV-2 positive as a result of exposure in hospital having presented with alternative diagnoses, and those under the age of 18 years were excluded. All patients were followed until death, discharge or the end of the study period on 27 April 2020.

Data collection


Individual electronic medical records (Cerner) of patients were reviewed and relevant parameters were manually extracted onto a structured collection database. Patient data on baseline demographics, body mass index, SARS-CoV-2 confirmation, comorbidities and admission medications were recorded analysing individual case records. Comorbidities were further confirmed by manual review of relevant correspondence in health records, especially if they were not clearly stated in the patient’s admission record. In-hospital course was reviewed, and data was collected on baseline heart rate, blood pressure, temperature and oxygen saturations on admission, requirement for respiratory support, echocardiographic parameters, initial and peak levels of prognostic biochemical markers, level of care required (intensive care vs ward based care) and in-hospital outcomes.

Myocardial injury was defined as a peak troponin greater than 99th percentile of the upper reference limit of high sensitivity troponin I (hs-TnI) (adjusted according to sex).

Pre-existing CVD was defined by the presence of hypertension, coronary artery disease (CAD)/ischaemic heart disease, valvular disease, impaired left ventricular (LV) function, arrhythmia, peripheral vascular disease or cerebrovascular disease. Patients were monitored for outcomes including death, discharge or continued inpatient treatment at the end of the monitoring period.

Patients or the public were not involved in the design, or conduct, or reporting, or dissemination plans of our research as it was a retrospective analysis and also to minimise interaction with COVID-19 patients.

Statistical analysis


The distributions of demographic characteristics, admission signs, pre-existing comorbidities, biomarkers (admission and peak) and the need for escalating levels of care were assessed for the whole cohort. These were then compared between those who died and those who remained alive at the end of the study using appropriate (parametric and non-parametric) tests of significance (see online supplemental table 5). Patients alive and continuing to require in-patient treatment were included in the alive group for baseline comparisons. Comorbidities were analysed separately for correlation with COVID-19 mortality, without combining into pre-existing comorbidity index such as the Charlson Score, as the relationship between COVID-19 and the separate elements of such risk scores is unknown. Logistic regression models were used to determine predictors of COVID-19 mortality. Patients continuing to require inpatient treatment at the end of the study were excluded from the regression modelling as their ultimate outcomes are unknown. In addition, variables which were poorly recorded (less than 80% completeness) were excluded as predictors. All analyses were carried out in SPSS V.24 and R V.3.6.3.

Results

Baseline Patient characteristics


A total of 498 patients were admitted to Imperial College Healthcare NHS trust between 7 March 2020 and 7 April 2020 with COVID-19-related symptoms. The mean age of the cohort was 67.4±16.1 years and 310 patients(62.2%) were male.

The most common comorbidities were hypertension (53.4%), diabetes (40.2%) and hyperlipidaemia (31.7%). 13.9% had a history of CAD, 6.6% had impaired LV function and 11.8% had a previous cerebrovascular accident. Chronic kidney disease (CKD) was seen in 19.7% of patients with 7.4% being on haemodialysis. The majority of patients were non-smokers (91.8%), with 12 patients(2.4%) and 29 patients (5.8%) being previous and current smokers respectively

On admission, 88 patients(17.7%) were on aspirin and 58 (11.6%) were anticoagulated. One hundred patients (20.1%) were on an ACE inhibitor (ACEi) and 52 (10.4%) on angiotensin receptor blockers (ARB).

Mortality

As of 27 April 2020, 462 patients (92.8%) out of 498 had completed outcomes. One hundred and fifty-four patients (30.9%) had died and 344 patients (69.1%) remained alive, of which 36 patients (10.5%) continued to require inpatient treatment.

The patients who died were older (74.3±13.4 years vs 64.1±16.2 years,p<0.001) with higher respiratory rates (25.9±11.3 vs 24.0±8.8,p=0.035) and lower oxygen saturations on air (91% (87–96) vs 94% (89–96),p=0.019) at presentation than those who remained alive at the end of the study

Patients with COVID-19 who died had higher incidence of pre-existing CVD (78.6% vs 57.6%, p<0.001), CKD (27.3% vs 16.3%, p=0.05), diabetes (46.8% vs 37.2%, p=0.048), hypertension (68.2% vs 46.8%, p=0.001) and end-stage renal failure (10.4% vs 6.1%, p=0.099) compared with those who remained alive.

Renin–angiotensin–aldosterone system blockade

Use of ARB therapy was not significantly higher in those who died when compared with those who remained alive (8.4% vs 11.3%,p=0.428). In contrast, patients who died were more likely to be taking ACEi (26.6% vs 17.2 %,p=0.021) .

In-hospital outcomes


In our patient cohort, 73 patients (14.7%) were admitted to intensive care unit (ICU) and 58 patients (11.6%) required intubation and ventilation. A total of 154 patients (30.9%) died in-hospital due to COVID-19.

Patients who died more frequently had acute myocardial injury (66.2% vs 32.8%, p<0.001), acute kidney injury (AKI) (39.0% vs 16.0%,p<0.001) and more commonly required renal replacement therapy (8.4% vs 3.5%, p=0.026) compared with those who remained alive. They were more frequently diagnosed with pneumonia (77.3% vs 62.2%, p=0.001)

Blood parameters

Admission and peak troponin levels, admission and peak d-dimer, B-type natriuretic peptide (BNP), C reactive protein (CRP) and creatinine were all significantly higher in patients who died in-hospital due to COVID-19 compared with those who were alive

Predictors of mortality

Myocardial injury (OR 2.39, 95% CI 1.31 to 4.40,p=0.005) and hypertension (OR 1.88, 95% CI 1.01 to 3.55,p=0.049) emerged as significant predictors of in-hospital mortality in adjusted analyses, each approximately doubling the odds of mortality when compared with demographically similar patients without myocardial injury or hypertension. In contrast, use ACEi became a non-significant predictor (p=0.095) once hypertension was accounted for

Myocardial injury


A total of 215 patients had myocardial injury (43%) based on their raised hs-TnI. The myocardial injury group has a higher proportion of patients with history of CVD (76.3% vs 54.8%,p<0.001), hypertension (64.2% vs 45.2%,p<0.001), previous MI (14.0% vs 5.3%,p=0.001), atrial fibrillation (19.1% vs 8.5%,p=0.001) and of patients taking ARB (14.4% vs 7.4%,p=0.017). Patients with myocardial injury had higher probability of death (47.4% vs 18.4%,p<0.001).

Cardiac intervention

Two hundred and fifteen patients (43.1%) had troponin elevation but only 11 patients (2.2%) were diagnosed as having acute coronary syndrome (ACS) and 9 patients (1.8%) were treated with dual antiplatelet therapy. Four patients were referred to our centres as STEMI patients with three of these cases taken to the cardiac catheter laboratory. Two of these STEMI cases needed percutaneous coronary intervention (PCI) (one following thrombolysis) and one had normal coronaries.

One of the STEMI case presented was a 60-year-old man with severe COVID-19 respiratory disease and was intubated within hours of admission. Five days after admission, he developed anterior ST elevation with raised troponin and D-Dimer. The patient was felt to be too unwell for a transfer across site and PCI and he was treated with thrombolysis. The patient improved after thrombolysis but then redeveloped ST changes 1 week later. His echocardiogram showed moderate LV impairment with anterior regional wall motion abnormality. He was then transferred to Hammersmith Hospital and underwent primary PCI with drug-eluting stents from his left main stem to left anterior descending (LAD). The patient was stable postprocedure and transferred back to ICU.

Thirty-four patients (6.8%) were reported to have inpatient arrhythmias with atrial fibrillation being the most frequent (online supplemental table 3). One patient was admitted with collapse and intermittent higher degree atrioventricular conduction block and required a permanent pacemaker. 35 patients (7.0%) had an inpatient echocardiogram which were focused scans to minimise risk to the operator (online supplemental table 4) of which 51.4% (18 patients) had normal echocardiograms. Two patients were diagnosed with myocarditis. One had a normal coronary angiogram, with ECG changes and troponin rise. The second patient had severely impaired LV function on a background of known previous LV impairment but developed recurrent supraventricular arrythmia needing amiodarone. One patient had cardiac MRI (cMRI) which showed multiple small areas of late gadolinium enhancement (LGE) subendocardially, consistent with small infarcts but also some mid-wall oedema and LGE more suggestive of a myocarditic process

Discussion

To our knowledge, this study represents the first case series of consecutive hospitalised confirmed COVID-19 patients in the UK describing cardiovascular outcomes. In-hospital mortality rate was 30.9% with 14.7% of patients being admitted to ICU. Our in-hospital mortality rate is comparable with published inpatient mortality of 28.2% in China and 21%–30% in the USA.2 6 7

We found that acute myocardial injury and history of hypertension significantly increased the odds of in-hospital mortality once other variables were accounted for.

CVD and myocardial injury

In our cohort, patients who died of COVID-19 had increased underlying CVD (78.6% vs 57.6%). Hypertension was the most common cardiovascular comorbidity present in 53.4% of patients and significantly predicted outcome. A large report from Chinese Center for Disease Control and Prevention looking at outcomes in 44 672 confirmed COVID-19 cases, reported overall mortality increasing from 2.3% to 10.5% in patients with CVD.8

Acute myocardial injury occurred in 43.2% of patients with raised hs-TnI levels. Patients who died from COVID-19 had higher rates of myocardial injury compared with those who survived (66.2% vs 32.8%) regardless of underlying CVD status. Chinese data has shown the SARS-CoV-2 infection causes myocardial injury and is associated with worse outcomes.3 4 One cohort of 416 COVID-19 patients showed that 82 (19.7%) patients had evidence of myocardial injury. Those with myocardial injury had a significantly higher associated in-hospital mortality (51.2%), compared with those without myocardial injury(4.5%).3 Guo et al reported 52 of 187 patients(27.8%) had raised troponin T (TnT) levels. In-hospital mortality was 59.6% (31 of 52) in those with raised TnT compared with those with normal levels, 8.9% (12 of 135).4 We have seen similar increased mortality of 47.4% in those with myocardial injury compared with 18.4% in those with normal troponin levels. The highest mortality rates were observed in those who had underlying CVD and raised TnT levels(69.4%).

Mechanisms of cardiac injury and impact on cardiovascular system


Patients with CAD and cardiovascular risk factors are at greater risk of cardiac events during acute infections and acute inflammatory conditions due to an increase in myocardial demand, causing myocardial injury or infarction in a type 2 myocardial infarction (MI) pattern.9–11 This is likely to be exacerbated by dehydration and acute kidney injury seen in many of the sickest patients in our cohort. Although severe inflammatory stress has been suggested to cause atherosclerotic plaque instability and rupture, we saw very little in the way of classical ACS or coronary artery plaque rupture in our patient cohort. Thromboembolic phenomena are thought to be associated with COVID-19 pathogenesis due to coagulopathy and endothelial dysfunction. This is reflected in raised troponin and D-Dimer levels. There have been suggestions that these may lead to coronary thromboembolism and present as ACS cases.12 In our cohort, only three STEMI cases had invasive coronary angiography and none were felt to be related to this phenomenon. One had normal coronary arteries. The two other cases had diffuse CAD, likely related to underlying atherosclerotic disease than acute thrombotic COVID-19-related pathology. Their underlying atherosclerotic disease could have been exacerbated by their acute infection. Italian data have suggested that up to 40% of COVID-19 STEMI patients have no identifiable coronary culprit lesion to explain abnormal ECG and troponin rise.13

Thirty-four patients (6.8%) were reported to have inpatient arrhythmias with atrial fibrillation being the most frequently observed rhythm, which is lower than the previously reported incidence of 16.7% by a Chinese group.14 As there appears to be no clear associated underlying ACS or LV dysfunction, these arrhythmias could be a consequence of severe underlying metabolic disturbances, hypoxia or severe inflammatory response.

Only 35 patients (7.0%) underwent focused echocardiography during their admission. These were focused scans in order to minimise contact with patients and reduce exposure to staff. Eighteen (51.4%) echocardiograms were normal (online supplemental table 3). Only four (0.8%) patients had moderate-severe LV impairment in our cohort. Despite significant number of patients with myocardial injury, there were no corresponding echocardiographic changes observed, suggesting troponin rise more likely related to inflammatory response than direct involvement of the myocardium. A Chinese study similarly reported that cardiac involvement was secondary to systemic involvement as patients failed to show any typical echocardiographic or ECG changes of myocarditis15

Due to the respiratory deterioration, some patients have shown radiological findings that may be consistent with pulmonary oedema. However, despite these patients having raised cardiac biomarkers, we have not seen the development of acute LV failure on echocardiography. Despite patients having no echocardiographic ventricular impairment, BNP was significantly raised in patients who died. This possibly indicates myocardial dysfunction that contributes to overall mortality.

There has been one case report in the literature identifying marked biventricular diffuse LGE and interstitial oedema on cMRI, consistent with acute myocarditis.16 Our cMRI findings suggest that there may be multiple modalities of cardiac involvement in COVID-19 rather than typical myocarditis.

In hypertensive patients, there is a higher expression of ACE2 and it has been suggested that this is the mechanism which may increase their susceptibility to SARS-CoV-2 infection. However, there is lacking clear evidence linking any direct causation.

ACEi and outcomes

SARS-CoV belongs to the β-CoVs group and binds to the zinc peptidase ACE2, a surface molecule to enter the host cell.17 18 Suppression of the ACE2 expression during SARS-CoV infection has been proposed to be involved in the pathogenesis of the disease in the lung, leading to severe infection and lung failure. ACEi/ARB can lead to increased upregulation of ACE2 receptors in the lungs which may contribute to lung pathology. Influenza A uses the same ACE2 receptor to mediate lung injury. A large UK analysis showed angiotensin blockade had no effect on influenza incidence or a lower incidence, depending on the duration of use.19 These observations for influenza may also apply to SARS-CoV-2. There are some suggestions that renin–angiotensin–inhibitors (ACEi/ARBs) may have a theoretical benefit, but clinical data is lacking.20 21 There have been concerns regarding the role renin–angiotensin–aldosterone system inhibitors have in COVID-19 patients. However, data from the USA, China and Italy have shown no association between ACEi/ARBs and COVID-19 mortality.22–25 Furthermore, there is at least one randomised control trial investigating the role of ACEi in COVID-19 (NCT04312009).

Although we found no mortality difference in patients on ACEi/ARB as a group, being on ACEi was linked to worse outcomes. Once this was adjusted for hypertension and myocardial injury, we found no increased mortality risk. However, we recognise our data represent a small patient group and current advice from international cardiology societies states that patients should remain on their medications until further definitive evidence is available. The role these medications play in the severity of lung disease is complex and not completely understood.

Cardiac management in COVID-19 patients

The mainstay of COVID-19 management has been respiratory support, predominantly in the form of intubation and ventilation.24 There has been very limited success to date in identifying any antiviral drugs or vaccines to target SARS-CoV-2.

Patients with CVD are at greater risk of myocardial injury and adverse outcomes. Cardiac biomarkers should be performed on all patients admitted with COVID-19 routinely, particularly those with underlying CVD. Despite these patients needing limited cardiac intervention, the cardiovascular system is significantly associated with mortality in COVID-19 patients. Increased troponin levels may help identify high-risk patients and may lead to modification in treatment strategy.

Importantly, cardiac issues may be masked as patients who present with significant respiratory symptoms can deteriorate rapidly before cardiac issues become apparent.

There were initial concerns that infected patients may present with a varied range of cardiac complications, including STEMI, arrhythmias and cardiomyopathy.26 In our cohort of patients, despite in-hospital mortality being associated with underlying CVD and myocardial injury, we did not observe high numbers of patients requiring catheter laboratory procedures as initially expected. Despite the numbers requiring intervention being low, we need to be aware that these patients may have underlying cardiac disease that needs intervention without which their prognosis may be worse. The two cases that needed PCI in our cohort had severe underlying three vessel disease which required intervention.

Our low number of cardiology interventions is likely to reflect the need to minimise patient contact due to the highly infectious nature of SARS-CoV-2. More importantly, patients presenting in a critical clinical status would not have benefited from cardiac intervention. Many institutes like ours have written thrombolysis protocols for STEMIs in COVID-19 positive patients. In our cohort of patients, only one case was administered thrombolysis (online supplemental table 1). The long-term consequences of conservative management in such patients is unknown, and this will require long term follow-up to ascertain potential long-term sequelae.

Limitations

Our study includes only 498 patients in 3 centres within a single NHS institution and larger cohort studies are needed to verify our findings. Our study was also limited to the geographical and ethnic population of North West London. Our analysis was retrospective and was limited to reviewing electronic patient records. We were limited by incomplete datasets available for patients. Data are lacking on long-term consequences of cardiac injury. Long-term observational studies are, therefore, required to understand this further and to explore the effectiveness in managing such patients.

Conclusion

Our study demonstrates that pre-existing CVD and age predict worse outcomes in patients hospitalised with COVID-19. Furthermore, biochemical myocardial injury is associated with increased mortality. Fewer patients than expected required cardiac intervention. Further studies are needed to investigate the long-term cardiovascular outcomes of patients who have survived COVID-19.
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