117 views | Akanimo Sampson | July 20, 2020
Around 20% of all COVID-19-associated deaths are said to be from cardiac complications.
This is coming as Nigeria on Sunday recorded 11 COVID-19 deaths which bring the national death toll to 789, and Edo State overtook Lagos in daily records of the virus cases, as the Nigeria Centre for Disease Control (NCDC), confirms fresh 556 cases.
Foreign Affairs Minister, Geoffrey Onyeama, has contracted the virus. According to him, “I did my fourth COVID-19 test yesterday at the first sign of throat irritation and unfortunately this time it came back positive. That is life! (You) win some, lose some. (I’m) heading for isolation in a health facility and praying for the best.”
While Onyeama is the first minister of President Muhammadu Buhari to test positive for COVID-19, the president last night wished him a quick recovery.
In a statement issued by his Senior Special Assistant on Media and Publicity, Garba Shehu, President Buhari described Onyeama as a strong pillar of his administration and commended him for tirelessly working to stem the spread of coronavirus in the country as a member of the Presidential Task Force on COVID-19, and ensuring the safety of Nigerians abroad.
“The country is eternally grateful to Geoffrey Onyeama for his diligence in attracting international support for Nigeria to defeat the coronavirus pandemic and boost the economy. I wish him a speedy recovery”, President Buhari says.
However, NCDC says till date, 36,663 COVID-19 cases have been confirmed, 15105 patients discharged, and 789 deaths recorded in 36 states and the Federal Capital Territory, Abuja.
Of the 556 new cases from 18 states, Edo recorded104 cases, Lagos-97, Abuja-70, Benue-66, Oyo-61, Kaduna-38, Plateau-28, Osun-19, Akwa Ibom-14, Rivers-13, Katsina-13, Ondo-13, Ogun-six, Kano-five, Nasarawa-four, Gombe-two, Ekiti-two, and Borno-one.
In the meantime, the mechanisms from which the cardiac complications arise have remained a topic of debate in the cardiology community.
One hypothesis centres on the infection of the heart itself, but the understanding of which cells may be infected is unclear.
To address this, Masonic Medical Research Institute (MMRI) Assistant Professor Dr Nathan Tucker, in collaboration with the Broad Institute, the University of Pennsylvania, and Bayer US, report the distribution of the SARS-CoV-2 receptor in a manuscript titled, “Myocyte upregulation of ACE2 in cardiovascular disease” published in the journal, Circulation.
MMRI is however dedicated to improving the health and quality of life for all humankind. The Institute’s primary mission is to conduct high quality basic biomedical and clinical research aimed at generating knowledge and information necessary for understanding molecular mechanisms of disease and development of medical cures and treatments of tomorrow.
The Institute is also committed to providing education and training to basic scientists, clinical researchers and students who will perpetuate and extend the fight against disease worldwide.
Its vision is to build scientific teams that can combine molecular biology, chemistry, computation, technology and engineering to create novel approaches to understanding and deciphering causes of disease. Using this knowledge, the Institute advances basic research to clinical application, therapeutics and cures.
To this end, the Institute will foster an environment of creativity, risk-taking, and open sharing of data and research. Finally, this new model will seek collaborations, both within the Institute and worldwide, in our mission to combat disease.
In the meantime, a large team of researchers with members affiliated with a host of institutions in France has identified what they believe is a hallmark of severe COVID-19 patients.
In their paper published in the journal Science, the group describes their study of 50 COVID-19 patients in France and what they learned from them.
The global pandemic has led medical scientists around the world to study the SARS-CoV-2 virus and associated infections. One characteristic of such infections is the difference in the degree of symptoms: some people are asymptomatic, while others find themselves unable to breathe.
Researchers are hoping that if the reason for different reactions to infection can be found, a means of treating people with severe infections may soon follow. In this new effort, the researchers studied 50 patients in French hospitals with varying symptoms—from those with a minor cough to those on ventilators.
Their goal was to find a common factor in patients with severe symptoms.
In analyzing blood, tissue, immune cells and other samples from the patients, the researchers came upon what they believe is a signature for people with severe infections—a combination of an interferon response deficiency and exacerbated inflammation.
They suggest the signature may represent a hallmark for severely ill COVID-19 patients. The researchers suggest their findings could lead to therapies that boost interferon response to infection while also reducing inflammation.
More specifically, the researchers found that critically ill patients had a deficiency in the response of type I interferons—a kind of protein that is used by the immune system to fight infections. In addition, there were higher than normal levels of proinflammatory signalling. Together, the two responses left patients with little ammunition to fight their infections.
The work builds on studies by other researchers finding that interferon signalling in infected areas may play a role in mitigating disease progression. Such work has shown that duration, timing and location of interferon exposure to the virus are critical factors that appear to underlie the degree of success with current therapies.
However, COVID-19 (SARS-CoV-2) infects cells through a particular cellular molecule, termed ACE2. To assess levels of this molecule in different patient populations and in response to common hypertension medications (ACE inhibitors), the group applied state-of-the-art single nucleus sequencing technologies in human heart samples.
From these studies, they were able to conclude that the amount of the viral receptor is increased in patients with pre-existing cardiac conditions, but only in the beating cells of the heart, termed cardiomyocytes.
Additionally, they found that the effect of anti-hypertension medications, termed ACE inhibitors, do not appreciably affect the levels of ACE2 in a way that would support any changes in the clinical use of these medications.
“This is but an early step in our understanding of cardiac pathology in people who contract COVID-19,” said Tucker, the first author of the manuscript.
“There’s much more work to do. As an example, we are already working to establish direct evidence of cardiac infection, while also examining receptor distributions in other populations and through other approaches. We hope to provide more information as soon as we are able.”
While just a piece in a very complex puzzle, this study offers a potential explanation as to why patients with pre-existing heart disease are more likely to suffer severe cardiac symptoms from COVID-19 infection. Importantly,
it also provides data on the effects of anti-hypertensive medications, supporting the previous statements urging continued use of ACE inhibitors from the American Heart Association, American College of Cardiology, and European Society of Cardiology with additional human-derived data.