ASCO 2020 virtual annual meeting – day 3

Our live coverage from this year’s slimmed down, virtual version of the American Society of Clinical Oncology (ASCO) annual meeting continues at 8am (ET) as we move into the third and final day of the oncology event.
It follows our live coverage of ASCO 2020 day 1 and day 2, during which we’ve already featured Amgen’s Kyprolis, AstraZeneca’s Tagrisso, rare cancers and genomics, BCMA therapy, COVID-19’s impact on cancer patients and much more.

View all the live coverage of the virtual ASCO 2020, and day three live blog is below (please allow the blog a few moments to load):

Last Updated: 38 minutes ago

38 minutes ago

J&J highlights data from lung cancer bispecific antibody

 richardstaines

Johnson & Johnson’s Janssen unit also has some interesting data from a bispecific antibody aimed at lung cancers with a mutation that renders approved targeted drugs useless.
Amivantamab was created in collaboration with its development partner Genmab and the latest data from Janssen came from a small study in non-small cell lung cancer with EGFR exon20 insertion mutations.
Data came from the study of 50 patients, of whom 39 were evaluable at data cut-off in October.
This showed an overall response rate of 36%, and 41% in patients who had already received platinum-based chemotherapy.
The clinical benefit rate was 67% overall and 72% for patients who had already received platinum chemo.
In the 14 responders, median duration of response was 10 months, with ongoing responses in nine patients at data cutoff.
Median progression-free survival was 8.3 months for response evaluable patients, and 8,6 months in those previously treated with platinum chemo.
In a briefing ahead of ASCO J&J pointed out that PFS is typically around 3.7 months in this patient group.
As there are no approved targeted therapies for this kind of lung cancer, the FDA has granted Breakthrough Therapy status to amivantamab in this form of lung cancer earlier this year.

an hour ago

Seeking novel therapies from the patient’s perspective

 Dominic_Tyer

Seeing a lot of positive comments about the Lost in the Woods? presentation on seeking novel therapies from the patient’s perspective from Dr Mark Lewis, director of gastrointestinal oncology at Intermountain Healthcare.
His take home points:
–       Don’t underestimate tech-savvy, self-advocating patients
–       Physicians – teach patients to use clinicaltrials.gov
–       Driver mutations are breaking down traditional histopathologic boundaries
–       The past was ‘shotgun’ toxicity, the future is ‘sniper’ aim
–       Patients are our partners in progress

2 hours ago

ASCO verdict on BMS’ first line lung cancer combination

 richardstaines

ASCO is saving its analysis of the ADAURA trial, the latest lung cancer data from AstraZeneca’s lung cancer drug Tagrisso (osimertinib) for its big plenary session in the afternoon.
But Benjamin Levy, clinical director of oncology at the Johns Hopkins Sidney Kimmel Cancer Center took us through the latest data from Bristol-Myers Squibb’s immunotherapy combination in first line lung cancer.
In the past few weeks BMS scored two FDA wins with the combination of Opdivo (nivolumab) and Yervoy (ipilimumab) in first line lung cancer.
An approval in first-line non-small cell lung cancer offered patients with the PD-L1 biomarker present in at least 1% of tumour cells the option of a chemotherapy-free regimen.
The other approval gave the option of Opdivo and Yervoy plus doublet chemotherapy regardless of the presence of PD-L1.
Levy’s conclusion is that these do offer two new options, although he cited concerns about the toxicity profile of the combination without chemotherapy, which caused 12% of patients to quit.
He wants to see five year data to select the best regimen in what is becoming a quite crowded field, with Merck & Co’s Keytruda (pembrolizumab) still the main contender.
He concluded with a lesson learned from AstraZeneca’s Imfinzi (durvalumab), which failed in the MYSTIC trial in first line lung cancer in 2017,.
Levy noted a 2018 exploratory analysis of the data showed “competitive outcomes” based on the plasma tumour mutation burden biomarker.
According to Levy this shows the “need to move beyond PD-L1 and find better biomarkers.”

[MORE]

https://pharmaphorum.com/oncology/asco-2020-virtual-meeting-day-3/

Thinking about thinking: lessons from the coronavirus

It’s been a rough few months for all of us—everyone, all over the whole world. I want to share a few thoughts on the coronavirus epidemic, politics, and what this reveals about human thinking.
For future reference, this is being written in late May 2020, and the U.S. is just now beginning to tentatively reopen after large sections of the country have been effectively quarantined. I’ve worked hard to be a relatively dispassionate observer of the developing dialog in the US, and, frankly, I’ve seen much that raises cause for concern. I’ll share some of these observations in a short series of blogs this week, and hopefully tie up with some ideas for how we can strengthen our rational abilities.
Though there’s always a lot going on, I see two critical influences in recent history:

• Over the past 10-15 years, the rise of social media
• Over the past 4-6 years, increasing political division, at least in the US and Europe

Let’s look at social media today, and we’ll consider the impact of politics in another post soon.

Social media

Social media is truly a mixed blessing. On one hand, we have easy interaction and some access to top experts in many fields. Of course, there are a host of people “hacking expertise” and pretending to be experts, but there’s at least the potential to access a richness and depth of thought that has never existed before.
However, from a practical perspective, this does not often happen, and the negatives often most strongly outweigh the positives.

Attention spans are cratering

For one thing, carefully engineered interfaces have changed human attention spans. We now click through stories and videos, sometime giving only a few seconds to snippets of information. This, of course, encourages the shallowest possible thinking, but the damage to our ability to focus may be catastrophic.
The best work humans can do is deep work, but how many people feel disconnected and disjointed today? How many people can sit down and focus on a task for hours? Is this different than it was just a decade ago? Where will we be ten years from now if this doesn’t change?
(As an aside, if you’re looking for hard research on this subject, the jury is still out. You can find studies that support what I’m saying, but other studies raise questions about methodology. Short answer is we don’t know, but I have a strong conviction, based on admittedly anecdotal evidence, that something is going on here.)

Find your echo chamber

One of the other issues in social media communities is that people tend to congregate in like-minded groups. Of course this makes sense, but is there a downside to being surrounded by people who think like you do?
You betcha. In reinforcing each other, these groups tend to defend their thinking. Good thinking means thinking about thinking—not an easy task. Confirmation bias works hard to “keep us in our lane” and blinds us to important pieces of information. In these small communities, the problem is often overwhelming.
Whether we realize it or not, our actions are the end result of evolution and tens of thousands of years of civilizations. Communities have existed to protect us from outsiders, from the proverbial barbarians coming over the hills. I worry this is misfiring in the social media environment, where communities so often insulate us from opinions and perspectives other than our own.
It might feel good to be in a group of people who agree with you, but being our best selves is often about being at least a little bit uncomfortable.

Constant emotional manipulation

It’s not about how we feel. Or is it?
Actually, social media engages in the war for our attention through primarily emotional means. Stories, pictures, and clickbait headlines are designed to grab attention and manipulate passions. Interactions on social media tend to go to “full on road rage” in seconds, perhaps because it’s easy to forget we are interacting with an actual human behind those glowing words on a screen.
How often have you seen an apparently rational person go off the deep end in just a few social media interchanges? It’s not unusual to see physical violence threatened, just because someone disagrees with an opinion. We could never get away with this in actual society, but social media is a great unknown, and that great unknown is a land of dialed up emotions and, often, dialed back reason.
That’s a good place to leave this today. In my next post, we’ll dig a little bit deeper into reason and emotion, and think about the part political beliefs play in this.

AdamHGrimes

Thinking about thinking: lessons from the coronavirus

State-Based Contact Tracing Apps Could Be a Mess

While governments around the world have launched nationwide Covid-19 contact-tracing smartphone apps over the last months, the US pointedly has not. Instead, it seems like the apps designed to detect coronavirus exposure stateside will launch on a state-by-state basis—and they may be anything but united.
When Google and Apple officially launched their exposure notification API for Android and iOS last week, their announcement included statements from three states—Alabama, North Dakota, and South Carolina—that are already building apps that will integrate the company’s Bluetooth-based system.
But it increasingly seems that neither the Centers for Disease Control and Prevention, nor the Department of Health and Human Services, nor any other US federal agency will release a nationwide coronavirus contact tracing app. “There is no effort I know of at the national level to build anything” like a contact tracing app, says someone familiar with the White House Covid-19 task force deliberations led by President Donald Trump’s son-in-law Jared Kushner, speaking to WIRED under the condition of anonymity. “Just like you’ve seen with the plan on testing and reopening, it’s being pushed to the states.”

 

Another adviser to that task force, Andy Slavitt, who led Medicare and Medicaid policy in the Obama administration and reportedly offered recommendations to Kushner, tells WIRED that any contact-tracing smartphone apps are almost certain to be left to the states alone. “I don’t think the federal government wants the responsibility to figure out the best and most efficient way to execute a contact tracing app,” says Slavitt. “If it’s like everything else they’re doing, they’re going to want to make sure the states have the responsibility.” Neither the CDC nor the HHS responded to WIRED’s request for comment about any plans to launch a national Covid-19 tracking or notification app.
“If this is getting done on a state-by-state level or even a confederacy of states, like the Western Pact, the question is then around security and interoperability,” says Ashkan Soltani, the former lead technologist for the Federal Trade Commission, who has been analyzing Covid-19 tracing and notification apps. “If each state is trying to put this together, you run the risk of commercial entities building this, the systems’ backends not being secure, and reliability issues.”

The potential for privacy disasters from contact tracing apps already have been well demonstrated. North Dakota’s app was found to be sharing data with Foursquare and Google’s advertising system. India’s contact tracing app made it possible to locate some Covid-19-infected users by spoofing GPS locations. And a flaw in Qatar’s contact tracing system leaked hundreds of thousands of users’ personal data, including health status and locations.
Rather than auditing one national app for security and privacy issues, Soltani says, every state-level contact tracing or exposure notification system will have to be individually vetted for those sorts of issues. And for each one, the devil will be in the details of its implementation.
Google and Apple’s Bluetooth-based system, for instance, offers app makers a relatively privacy-preserving approach: It doesn’t collect any location information from phones, and doesn’t even collect any information at all from the phones of users who don’t voluntarily mark themselves as having been diagnosed as Covid-19 positive. For the vast majority of users, no information is ever uploaded to the server of the organization running the app.
But when a Covid-19 patient self-reports as positive through the system, their apps upload a set of rotating codes that their phones have transmitted to other users via Bluetooth for the previous two weeks. While those codes aren’t identifying in themselves, every app maker will have to take care not to collect the IP addresses of those Covid-19 patients’ smartphones, which could be used to identify infected individuals. Or if they do collect those IP addresses—say, to prevent denial of service attacks on their servers—they’ll have to be careful not to keep the data for too long or allow it to leak.

Those sorts of implementation issues only become more critical if some states choose to use other systems that, unlike the one designed by Google and Apple, instead collect location information—as the contact tracing app launched in the state of Utah does. That could potentially leave state agencies responsible for protecting sensitive information about the movements of millions of people. “I definitely don’t trust 50 different state health departments to do this as reliably as one federal agency,” says Matthew Green, a cryptographer at Johns Hopkins who has analyzed the security of contact tracing and exposure notification apps.
More fundamentally, Green argues, a state-by-state approach raises the potential for states to use different, incompatible systems, so that Covid-19 exposure events might be missed if a user crosses state lines. “If I’m in New York and a lot of people are coming in from New Jersey, it seems like it’s going to be a big problem,” he adds. “It’s the opposite of a network effect.”
Green notes that if two states’ apps are both using Google and Apple’s protocol, that interoperability problem becomes more manageable. The two states simply share the unique codes that have been uploaded by Covid-19 positive users, so that people who have come into Bluetooth proximity with them in either state can be warned. Apple and Google have even suggested that multiple states’ apps could be designed to run on the same backend server infrastructure.
But that interoperability falls apart if one state, like Utah, opts for a location-based system, while others are using a Bluetooth-based one—or even if one state is using a decentralized Bluetooth-based system like the Google and Apple system, while another deploys a centralized model implemented by countries like Australia and Singapore. “It’s very easy to make decentralized apps interoperable,” says Cristina White, a Stanford professor and executive director of the decentralized exposure notification system CovidWatch. “If everyone is doing different things, with some decentralized and some centralized, and everyone’s using different protocols, that’s harder.”

Another contact-tracing app project, the MIT spinoff nonprofit Pathcheck, says it’s currently in talks with a dozen states or “jurisdictions”—multistate regions—about rolling out contact tracing or exposure notification apps for those areas. But MIT professor Ramesh Rashkar, one of the group’s founders, says that most of the agencies he’s talked to have expressed more interest in location-based contact tracing apps than in the Bluetooth-based system developed by by Google and Apple. And he concedes that could create interoperability issues until a standard is established. “My expectation is that in the immediate version, there’ll be a mess with the respect to interoperability, but that it will get fixed as we deploy more solutions,” adds Rashkar.
Contact tracing and exposure notification apps, regardless, represent at best one tool that can help Americans return to normal life. Slavitt, the Obama-era health care czar, says that, for instance, he sees the apps as “between 10 and 20 percent” of a larger picture depending far more on manual contact tracing and widespread testing.
But now, with no nationwide app in the US, fragmentation threatens to become another hurdle to even such a relatively modest role for Covid-19 alert and tracking apps. Until states can agree on a standard or build interoperability between their systems, every line on the US map could represent another constraint on a technology that might otherwise help chip away at the global pandemic’s effects.
https://www.wired.com/story/covid-19-contact-tracing-app-fragmentation/

Protesters increase the risk of getting, spreading coronavirus: officials

Protesters flooding streets across America are putting themselves at risk of catching the coronavirus — and likely exacerbating its ongoing spread, officials have warned.
“If you were out protesting last night, you probably need to go get a COVID test this week,” Atlanta Mayor Keisha Lance Bottoms warned those taking to the streets in her city.
Bottoms was one of many to note the dangers of thousands suddenly ignoring any form of lockdown or social distancing to protest George Floyd’s caught-on-camera death in police custody.
She stressed that “there is still a pandemic in America that’s killing black and brown people at higher numbers.”
Health experts fear that silent carriers of the virus who have no symptoms could unwittingly infect others at protests where people are packed cheek to jowl, many without masks.
Even those with masks are not guaranteed protection, with the Centers for Disease Control and Prevention (CDC) saying cloth masks are more for stopping infected people spreading the virus than protecting the wearer.

 

“Whether they’re fired up or not, that doesn’t prevent them from getting the virus,” warned Bradley Pollock, chairman of the Department of Public Health Sciences at the University of California, Davis.
The protests are almost certainly going to fuel infections and damage efforts to contain the pandemic through lockdowns and tightly organized social distancing, Minnesota’s health commissioner warned.
“We have two crises that are sandwiched on top of one other,” said Jacob Frey, the mayor of Minneapolis where Floyd died during the Memorial Day arrest.
The ongoing protests come as the US has seen more than 1.7 million confirmed coronavirus cases with 103,781 deaths, according to a tally by Johns Hopkins University.
https://nypost.com/2020/05/31/protesters-have-increased-risk-of-getting-coronavirus-officials/

Russia OKs flu drug for COVID-19

Russia’s Ministry of Health has approved an off-patent pill, originally sold under the brand name Avigan for influenza by a unit of Fujifilm Holdings (OTCPK:FUJIF), for the treatment of hospitalized COVID-19 patients.

Early tests showed that the antiviral, favipiravir, shortened recovery time. In the first randomized trial, 65% (n=26/40) of treated patients tested negative for the virus within five days, about half the time it took untreated patients to recover. It works by interfering with the ability of RNA viruses to replicate.

Western scientists say they want to review the data before judging whether other countries should add the med to their COVID-19 armamentaria.

Investigators in Japan and China are currently testing favipiravir’s effect on the coronavirus. The former’s trial sites include three locations in Massachusetts. The White House has indicated a keen interest in pushing its use in the U.S.

Gilead Sciences’ (NASDAQ:GILD) remdesivir, OK’d by the FDA for emergency use on May 1, is an injectable and remains the only drug approved thus far in America for for the respiratory disease.

https://seekingalpha.com/news/3578839-russia-oks-flu-drug-for-covidminus-19

Amazon scales back deliveries near protests

As the death of George Floyd sparks demonstrations across the country, Amazon (NASDAQ:AMZN) is scaling back deliveries and adjusting routes in a number of cities including Chicago, Los Angeles and Portland.

The e-commerce giant is “in close contact with local officials” and will only reopen delivery stations when it can “ensure the safety of our teams.”

https://seekingalpha.com/news/3578835-amazon-scales-back-deliveries-near-protests

Coronavirus May Be a Blood Vessel Disease, Which Explains Everything

In April, blood clots emerged as one of the many mysterious symptoms attributed to Covid-19, a disease that had initially been thought to largely affect the lungs in the form of pneumonia. Quickly after came reports of young people dying due to coronavirus-related strokes. Next it was Covid toes — painful red or purple digits.

What do all of these symptoms have in common? An impairment in blood circulation. Add in the fact that 40% of deaths from Covid-19 are related to cardiovascular complications, and the disease starts to look like a vascular infection instead of a purely respiratory one.

Months into the pandemic, there is now a growing body of evidence to support the theory that the novel coronavirus can infect blood vessels, which could explain not only the high prevalence of blood clots, strokes, and heart attacks, but also provide an answer for the diverse set of head-to-toe symptoms that have emerged.

“All these Covid-associated complications were a mystery. We see blood clotting, we see kidney damage, we see inflammation of the heart, we see stroke, we see encephalitis [swelling of the brain],” says William Li, MD, president of the Angiogenesis Foundation. “A whole myriad of seemingly unconnected phenomena that you do not normally see with SARS or H1N1 or, frankly, most infectious diseases.”

“If you start to put all of the data together that’s emerging, it turns out that this virus is probably a vasculotropic virus, meaning that it affects the [blood vessels],” says Mandeep Mehra, MD, medical director of the Brigham and Women’s Hospital Heart and Vascular Center.

In a paper published in April in the scientific journal The Lancet, Mehra and a team of scientists discovered that the SARS-CoV-2 virus can infect the endothelial cells that line the inside of blood vessels. Endothelial cells protect the cardiovascular system, and they release proteins that influence everything from blood clotting to the immune response. In the paper, the scientists showed damage to endothelial cells in the lungs, heart, kidneys, liver, and intestines in people with Covid-19.

“The concept that’s emerging is that this is not a respiratory illness alone, this is a respiratory illness to start with, but it is actually a vascular illness that kills people through its involvement of the vasculature,” says Mehra.

A respiratory virus infecting blood cells and circulating through the body is virtually unheard of.

A one-of-a-kind respiratory virus

SARS-CoV-2 is thought to enter the body through ACE2 receptors present on the surface of cells that line the respiratory tract in the nose and throat. Once in the lungs, the virus appears to move from the alveoli, the air sacs in the lung, into the blood vessels, which are also rich in ACE2 receptors.

“[The virus] enters the lung, it destroys the lung tissue, and people start coughing. The destruction of the lung tissue breaks open some blood vessels,” Mehra explains. “Then it starts to infect endothelial cell after endothelial cell, creates a local immune response, and inflames the endothelium.”

A respiratory virus infecting blood cells and circulating through the body is virtually unheard of. Influenza viruses like H1N1 are not known to do this, and the original SARS virus, a sister coronavirus to the current infection, did not spread past the lung. Other types of viruses, such as Ebola or Dengue, can damage endothelial cells, but they are very different from viruses that typically infect the lungs.

Benhur Lee, MD, a professor of microbiology at the Icahn School of Medicine at Mount Sinai, says the difference between SARS and SARS-CoV-2 likely stems from an extra protein each of the viruses requires to activate and spread. Although both viruses dock onto cells through ACE2 receptors, another protein is needed to crack open the virus so its genetic material can get into the infected cell. The additional protein the original SARS virus requires is only present in lung tissue, but the protein for SARS-CoV-2 to activate is present in all cells, especially endothelial cells.

“In SARS1, the protein that’s required to cleave it is likely present only in the lung environment, so that’s where it can replicate. To my knowledge, it doesn’t really go systemic,” Lee says. “[SARS-CoV-2] is cleaved by a protein called furin, and that’s a big danger because furin is present in all our cells, it’s ubiquitous.”

Endothelial damage could explain the virus’ weird symptoms

An infection of the blood vessels would explain many of the weird tendencies of the novel coronavirus, like the high rates of blood clots. Endothelial cells help regulate clot formation by sending out proteins that turn the coagulation system on or off. The cells also help ensure that blood flows smoothly and doesn’t get caught on any rough edges on the blood vessel walls.

“The endothelial cell layer is in part responsible for [clot] regulation, it inhibits clot formation through a variety of ways,” says Sanjum Sethi, MD, MPH, an interventional cardiologist at Columbia University Irving Medical Center. “If that’s disrupted, you could see why that may potentially promote clot formation.”

Endothelial damage might account for the high rates of cardiovascular damage and seemingly spontaneous heart attacks in people with Covid-19, too. Damage to endothelial cells causes inflammation in the blood vessels, and that can cause any plaque that’s accumulated to rupture, causing a heart attack. This means anyone who has plaque in their blood vessels that might normally have remained stable or been controlled with medication is suddenly at a much higher risk for a heart attack.

“Inflammation and endothelial dysfunction promote plaque rupture,” Sethi says. “Endothelial dysfunction is linked towards worse heart outcomes, in particular myocardial infarction or heart attack.”

Blood vessel damage could also explain why people with pre-existing conditions like high blood pressure, high cholesterol, diabetes, and heart disease are at a higher risk for severe complications from a virus that’s supposed to just infect the lungs. All of those diseases cause endothelial cell dysfunction, and the additional damage and inflammation in the blood vessels caused by the infection could push them over the edge and cause serious problems.

The theory could even solve the mystery of why ventilation often isn’t enough to help many Covid-19 patients breathe better. Moving air into the lungs, which ventilators help with, is only one part of the equation. The exchange of oxygen and carbon dioxide in the blood is just as important to provide the rest of the body with oxygen, and that process relies on functioning blood vessels in the lungs.

“If you have blood clots within the blood vessels that are required for complete oxygen exchange, even if you’re moving air in and out of the airways, [if] the circulation is blocked, the full benefits of mechanical ventilatory support are somewhat thwarted,” says Li.

A new paper published last week in the New England Journal of Medicine, on which Li is a co-author, found widespread evidence of blood clots and infection in the endothelial cells in the lungs of people who died from Covid-19. This was in stark contrast to people who died from H1N1, who had nine times fewer blood clots in the lungs. Even the structure of the blood vessels was different in the Covid-19 lungs, with many more new branches that likely formed after the original blood vessels were damaged.

“We saw blood clots everywhere,” Li says. “We were observing virus particles filling up the endothelial cell like filling up a gumball machine. The endothelial cell swells and the cell membrane starts to break down, and now you have a layer of injured endothelium.”

Finally, infection of the blood vessels may be how the virus travels through the body and infects other organs — something that’s atypical of respiratory infections.

“Endothelial cells connect the entire circulation [system], 60,000 miles worth of blood vessels throughout our body,” says Li. “Is this one way that Covid-19 can impact the brain, the heart, the Covid toe? Does SARS-CoV-2 traffic itself through the endothelial cells or get into the bloodstream this way? We don’t know the answer to that.”

In another paper that looked at nearly 9,000 people with Covid-19, Mehra showed that the use of statins and ACE inhibitors were linked to higher rates of survival.

If Covid-19 is a vascular disease, the best antiviral therapy might not be antiviral therapy

An alternative theory is that the blood clotting and symptoms in other organs are caused by inflammation in the body due to an over-reactive immune response — the so-called cytokine storm. This inflammatory reaction can occur in other respiratory illnesses and severe cases of pneumonia, which is why the initial reports of blood clots, heart complications, and neurological symptoms didn’t sound the alarm bells. However, the magnitude of the problems seen with Covid-19 appear to go beyond the inflammation experienced in other respiratory infections.

“There is some increased propensity, we think, of clotting happening with these [other] viruses. I think inflammation in general promotes that,” Sethi says. “Is this over and above or unique for SARS-CoV-2, or is that just because [the infection] is just that much more severe? I think those are all really good questions that unfortunately we don’t have the answer to yet.”

Anecdotally, Sethi says the number of requests he received as the director of the pulmonary embolism response team, which deals with blood clots in the lungs, in April 2020 was two to three times the number in April 2019. The question he’s now trying to answer is whether that’s because there were simply more patients at the hospital during that month, the peak of the pandemic, or if Covid-19 patients really do have a higher risk for blood clots.

“I suspect from what we see and what our preliminary data show is that this virus has an additional risk factor for blood clots, but I can’t prove that yet,” Sethi says.

The good news is that if Covid-19 is a vascular disease, there are existing drugs that can help protect against endothelial cell damage. In another New England Journal of Medicine paper that looked at nearly 9,000 people with Covid-19, Mehra showed that the use of statins and ACE inhibitors were linked to higher rates of survival. Statins reduce the risk of heart attacks not only by lowering cholesterol or preventing plaque, they also stabilize existing plaque, meaning they’re less likely to rupture if someone is on the drugs.

“It turns out that both statins and ACE inhibitors are extremely protective on vascular dysfunction,” Mehra says. “Most of their benefit in the continuum of cardiovascular illness — be it high blood pressure, be it stroke, be it heart attack, be it arrhythmia, be it heart failure — in any situation the mechanism by which they protect the cardiovascular system starts with their ability to stabilize the endothelial cells.”

Mehra continues, “What we’re saying is that maybe the best antiviral therapy is not actually an antiviral therapy. The best therapy might actually be a drug that stabilizes the vascular endothelial. We’re building a drastically different concept.”

https://elemental.medium.com/coronavirus-may-be-a-blood-vessel-disease-which-explains-everything-2c4032481ab2