Coronavirus can break your heart / Heart - related study

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

Post by trader32176 »

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 ... 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

Post by trader32176 »

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

11/8/20 ... 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.


COVID-19 Dashboard by the Center for Systems Science and Engineering (CSSE) at Johns Hopkins University (JHU) - ... 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. ... 4.364315v1
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Re: Coronavirus can break your heart / Heart - related study

Post by trader32176 »

Study investigates link between myocarditis and COVID-19

11/19/20 ... 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

Post by trader32176 »

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

1/11/21 ... -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


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

Post by trader32176 »

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

1/11/21 ... 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."


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.
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