Via Kevin Drum at Mother Jones the other day: two news reports on the novel coronavirus show why this isn‘t just a fancy version of the flu. This isn’t the newest news, but the picture gets bigger every day.
Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19)
Question What are the cardiovascular effects in unselected patients with recent coronavirus disease 2019 (COVID-19)?
Findings In this cohort study including 100 patients recently recovered from COVID-19 identified from a COVID-19 test center, cardiac magnetic resonance imaging revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), which was independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis.
Meaning These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19.
Caveat: this is a study of 100 patients in Germany. It should be taken as a call for further research. There’s not enough of a sample size across a broad enough population to reach general conclusions — but roughly two thirds of the people who were infected developed inflammation of the heart. That’s enough to warrant looking farther.
These were patients who had recovered from the infection; it shows that the virus affects the heart as well as the respiratory system and that the effects can persist even though the patient is otherwise apparently recovered.
Are the cardiac effects temporary? How severe is the damage? How long does it last, and what are the long term consequences? How many people are asymptomatic, but have had heart or other damage without knowing it? It’s a novel virus, meaning we are still finding out.
Drum’s second linked article adds more to the picture — how is the virus doing this?
We Thought It Was Just a Respiratory Virus. We were wrong.
This article in the University of California San Francisco Magazine discusses all the different ways the virus seems to attack the body, and why it’s more than just a respiratory virus. What seems to be a key tool for the virus is its ability to grab onto ACE2 receptors on the surface of cells, and use them as an entry point.
The novel coronavirus, an RNA virus named SARS-CoV-2, has become notorious for its skill at breaking and entering human cells. Its tools of choice are the protein spikes protruding from its surface – a feature that distinguishes all coronaviruses. The spikes of SARS-CoV-2 are the crème de la crème: By the luck of the evolutionary draw, they are able to easily grab hold of protein gates on human cells known as ACE2 receptors and, like jackknives, pry these gates open.
The heart is rich with ACE2 receptors, which may help explain the cardiac complications of the virus; but those receptors are also found on other cells. That seems to explain people suffering symptoms that show up in different ways:
In late January, when hospitals in the United States confirmed the presence of the novel coronavirus, health workers knew to watch for precisely three symptoms: fever, cough, and shortness of breath. But as the number of infections climbed, the symptom list began to grow. Some patients lost their sense of smell and taste. Some had nausea or diarrhea. Some had arrhythmias or even heart attacks. Some had damaged kidneys or livers. Some had headaches, blood clots, rashes, swelling, or strokes. Many had no symptoms at all.
It’s not just that the virus can destroy cells. (Indeed — some experiments show it doesn’t seem to kill cells outright.) What is still being determined is how it also sometimes triggers an immune response by the body that wreaks the real damage.
Or — a non-response where nothing at all appears to happen.
Most likely, though, you won’t feel sick at all. When UCSF researchers tested people for SARS-CoV-2 in San Francisco’s Mission District, 53% of those infected never had any symptoms. “That’s much higher than expected,” says Monica Gandhi, MD, MPH, a UCSF professor of medicine with expertise in HIV. Surveys of outbreaks in nursing homes and prisons show similar or even higher numbers. “If we did a mass testing campaign on 300 million Americans right now, I think the rate of asymptomatic infection would be somewhere between 50% and 80% of cases,” Gandhi says. Millions of people may be spreading the virus without knowing it, she points out, making asymptomatic transmission the Achilles’ heel of efforts to control the pandemic – and highlighting the importance of universal masking.
Reading the entire UCSF article, the picture painted of the virus is as a pathogenic multi-tasker. It’s capable of attacking a variety of systems in the body, triggering an over-reaction from the immune system, spreading aggressively because it often fails to produce symptoms, and persisting in some people for weeks or months. Again, we simply don’t know what kind of long term health effects the virus may produce — because we’ve been dealing with it for less than a year. This creates huge uncertainties for healthcare in the years ahead.
Bottom line — we have to take every precaution we can, and invest in testing and tracing. Until there’s a vaccine, that’s the least we can do.
Of course we have some huge uncertainties much closer to hand.
There’s been a determined effort to dismiss Covid-19 as just a cold with ambition, no worse than the flu. Trump, the GOP and death cult conservatives like Limbaugh are desperate to make people stop worrying about it, even with the death toll up to 150,000 in the USA and no end in sight. They are essentially promoting human sacrifice, trying to send people back to work and children back to school to restart the economy again so Trump can win in November. Or so they hope...
Good luck with that economy. How bad is it? This bad.