Tom Sizemore dead at 61

‘Saving Private Ryan’ and ‘Black Hawk Down’ star has been in critical condition. Sizemore’s family were informed by doctors earlier this week ‘there is no further hope’

Tom Sizemore, the actor known for portraying Mike Horvath in “Saving Private Ryan,” has died, Fox News Digital confirmed. He was 61.

“It is with great sadness and sorrow I have to announce that actor Thomas Edward Sizemore (“Tom Sizemore”) aged 61 passed away peacefully in his sleep today at St Joseph’s Hospital Burbank,” Sizemore’s representative Charles Lago said in a statement to Fox News Digital.

“His brother Paul and twin boys Jayden and Jagger, 17, were at his side.”

Lago continued, “In the early hours of Saturday, February 18, 2023, Tom Sizemore collapsed at his Los Angeles home and was transported to a hospital by Paramedics. He was found to be suffering from a brain aneurysm that occurred as a result of a stroke. Since that day, Tom has remained in critical condition, in a coma and in intensive care. Tom has remained in intensive care since that day and not regained conciseness.”

Tom Sizemore, the actor known for portraying Mike Horvath in “Saving Private Ryan,” has died, we can confirm. He was 61. (Jeff Vespa)

“There will be a private cremation service for the family with a larger celebration of life event planned in a few weeks.”

“The Sizemore family has been comforted by the hundreds of messages of support and love shown to their son, brother and father. They are asking for privacy during this difficult time and I am asking for those wishes to please be respected.”

“On a personal note, I am very saddened by the loss of not only a client but a great friend and mentor of almost 15 years. Tom was one of the most sincere, kind and generous human beings I have had the pleasure of knowing. His courage and determination through adversity was always an inspiration to me. The past couple of years were great for him and he was getting his life back to a great place. He loved his sons and his family. I will miss my friend Tom Sizemore Greatly.”

Lago also provided a statement on behalf of Sizemore’s ex-wife Maeve Quinlan, to whom he was married from 1996 to 1999 and who remained in contact with the late actor.

“My heartfelt condolences to the entire Sizemore family and Tom’s long-time manager, Charles Lago,” Quinlan said. “Most especially, my thoughts and prayers go out to Tom’s two sons, Jayden and Jagger. May God hold you both in the palm of his hand, give you strength and bless you all the days of your lives.”

“I am deeply saddened by the loss of my big brother Tom,” Sizemore’s brother Paul Sizemore said in a statement provided by Lago.

Paul continued, “He was larger than life. He has influenced my life more than anyone I know. He was talented, loving, giving and could keep you entertained endlessly with his wit and storytelling ability. I am devastated he is gone and will miss him always”

Lago added, “The twins are devastated by the loss of their father and will release a statement at a later time. I ask that the boys are afforded privacy during this very difficult [time].”

Sizemore was hospitalized on Feb. 18 after suffering a brain aneurysm that occurred as a result of a stroke, his representative previously confirmed to Fox News Digital. (Tibrina Hobson)

Sizemore was hospitalized on Feb. 18 after suffering a brain aneurysm that occurred as a result of a stroke, Lago previously confirmed to Fox News Digital. He was placed in critical condition and was receiving intensive care at the hospital.

“His family is aware of the situation and are hoping for the best,” Lago said at the time. “It is too early to know about [a] recovery situation as he is in critical condition and under observation.”

On Feb. 27, things took a turn for the worse, with Lago confirming, “Doctors informed his family that there is no further hope and have recommended end-of-life decision.”

“The family is now deciding end-of-life matters.”

Per Mayo Clinic, a brain aneurysm is described as the “bulge or ballooning in a blood vessel in the brain” that “can leak or rupture, causing bleeding into the brain (hemorrhagic stroke).”Sizemore enjoyed a successful run in Hollywood in the late 1990s to early 2000s starring in blockbuster films including “Black Hawk Down” and “Heat” His career then took a hit following issues with substance abuse and arrests for DUI, domestic abuse, and possession of a controlled substance.

In 2013, he released a memoir detailing his “wild ride through Hollywood,” titled, “By Some Miracle I Made It Out of There.”

On Feb. 27, things took a turn for the worse, with Sizemore’s rep confirming, “Doctors informed his family that there is no further hope and have recommended end-of-life decision.” (Robin Marchant)

A synopsis of the book said Sizemore’s days had been “filled with overdoses, suicide attempts, and homelessness.”

The memoir was “a harrowing journey into the heart of his addiction, told in riveting and often shocking detail. By turns gritty and heartbreaking, it is also one man’s look at a particular moment in entertainment history—a window into the drug-fueled spotlight that sent Robert Downey, Jr., to jail and killed River Phoenix, Heath Ledger, Chris Farley, and many others far before their time.”

Born in Detroit, Sizemore, starred in films including “Born on the Fourth of July” with Tom Cruise, “Pearl Harbor” with Ben Affleck, and the television show “Twin Peaks“.

According to IMDb, the actor currently has 33 upcoming credits for various productions.

In 2013, he released a memoir detailing his “wild ride through Hollywood,” titled, “By Some Miracle I Made It Out of There.” (CBS)

Sizemore worked with Tom Hanks and Matt Damon in Steven Spielberg’s World War II drama, “Saving Private Ryan.” (CBS Photo Archive)

He has also produced and written a variety of projects.

Previously married to actress Maeve Quinlan from 1996 through 1999, Sizemore had several run-ins with the law and openly discussed his journey to sobriety.

In an interview with Fox News Digital in 2021, Sizemore shared his commitment to getting sober, saying “I’ve been trying to get sober since 1991 … It became really big news much later than that, but I was trying to stop. I’ve had a problem for a long time. I had periods, long periods, of sobriety and I would end up relapsing.”

Tom Sizemore had more than 200 film and television credits to his name. (Mike Nelson)

“I still go to meetings and work my steps, but I had reached a place in my life where I knew I had to stop,” he explained. “I couldn’t be arrogant anymore. If I wanted to reach a nice and pleasant old age, I had to stop. And if I wanted to watch my kids grow up, I needed to reach a place where I knew it was over.”

By Haley Chi-Sing , Caroline Thayer , Ashley Hume

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Tom Sizemore, ‘Saving Private Ryan’ Actor, Dies at 61 after suffering brain aneurysm

LOS ANGELES (AP) – Tom Sizemore, the “Saving Private Ryan” actor whose bright 1990s star burned out under the weight of his own domestic violence and drug convictions, died Friday at age 61.

The actor had suffered a brain aneurysm on Feb. 18 at his home in Los Angeles. He died in his sleep Friday at a hospital in Burbank, California, his manager Charles Lago said.

Sizemore became a star with acclaimed appearances in “Natural Born Killers” and the cult-classic crime thriller “Heat.” But serious substance dependency, abuse allegations and multiple run-ins with the law devastated his career, left him homeless and sent him to jail.

As the global #MeToo movement wave crested in late 2017, Sizemore was also accused of groping an 11-year-old Utah girl on set in 2003. He called the allegations “highly disturbing,” saying he would never inappropriately touch a child. Charges were not filed.

he was part of the voice cast for 2002’s “Grand Theft Auto: Vice City” video game

Despite the raft of legal trouble, Sizemore had scores of steady film and television credits — though his career never regained its onetime momentum. Aside from “Black Hawk Down” and “Pearl Harbor,” most of his 21st century roles came in low-budget, little-seen productions where he continued to play the gruff, tough guys he became famous for portraying.

“I was a guy who’d come from very little and risen to the top. I’d had the multimillion-dollar house, the Porsche, the restaurant I partially owned with Robert De Niro,” the Detroit-born Sizemore wrote in his 2013 memoir, “By Some Miracle I Made It Out of There.” “And now I had absolutely nothing.”

The book’s title was taken from a line uttered by his character in “Saving Private Ryan,” a role for which he garnered Oscar buzz. But he wrote that success turned him into a “spoiled movie star,” an “arrogant fool” and eventually “a hope-to-die addict.”

He racked up a string of domestic violence arrests. Sizemore was married once, to actor Maeve Quinlan, and was arrested on suspicion of beating her in 1997. While the charges were dropped, the couple divorced in 1999.

Sizemore was convicted of abusing ex-girlfriend Heidi Fleiss in 2003 — the same year he pleaded no contest and avoided trial in a separate abuse case — and sentenced to jail. The former Hollywood madam testified that he had punched her in the jaw at a Beverly Hills hotel, and beaten her in New York to the point where they couldn’t attend the “Black Hawk Down” premiere.

The sentencing judge said drug abuse was likely a catalyst but that testimony had revealed a man who had deep problems dealing with women. Fleiss called Sizemore “a zero” in a conversation with The Associated Press after his conviction.

Sizemore apologized in a letter, saying he was “chastened” and that “personal demons” had taken over his life, though he later denied abusing her and accused her of faking a picture showing her bruises.

Fleiss also sued Sizemore, saying she suffered emotional distress after he threatened to get her own probation revoked. Fleiss had been convicted in 1994 of running a high-priced call-girl ring. That lawsuit was settled on undisclosed terms.

Sizemore was the subject of two workplace sexual harassment lawsuits related to the 2002 CBS show “Robbery Homicide Division,” in which he played a police detective. He was arrested as recently as 2016 in another domestic violence case.

Sizemore ended up jailed from August 2007 to January 2009 for failing numerous drug tests while on probation and after Bakersfield, California, authorities found methamphetamine in his car.

“God’s trying to tell me he doesn’t want me using drugs because every time I use them I get caught,” Sizemore told The Bakersfield Californian in a jailhouse interview.

Sizemore told the AP in 2013 that he believed his dependency was related to the trappings of success. He struggled to maintain his emotional composure as he described a low point looking in the mirror: “I looked like I was 100 years old. I had no relationship with my kids; I had no work to speak off. I was living in squat.”

He appeared on the reality TV show “Celebrity Rehab” and its spinoff “Sober House,” telling the AP that he did the shows to receive help, but also partly to pay off accumulated debts that ran into the millions.

Many of Sizemore’s later-career films had a sci-fi, horror or action bent: In 2022 alone, he starred in movies with such titles as “Impuratus,” “Night of the Tommyknockers” and “Vampfather“. But Sizemore still nabbed a few meaty roles — including in the “Twin Peaks” revival — and guest spots on popular shows like “Entourage” and “Hawaii Five-O“.

A stuntman sued Sizemore and Paramount Pictures in 2016, saying he was injured when the allegedly intoxicated actor ran him over while filming USA’s “Shooter“. State records obtained by the AP showed that Sizemore was only supposed to be sitting in the unmoving car and that he “improvised at the end of the scene and drove away in his car.” Sizemore was fired from “Shooter” and the stuntman’s lawsuit was settled on undisclosed terms.

In addition to his film and TV credits, he was part of the voice cast for 2002’s “Grand Theft Auto: Vice City” video game. He also taught classes at the LA West Acting Studio, according to recent advertisements.

He is survived by his 17-year-old twin sons, Jayden and Jagger, and his brother Paul, all of whom were by his side when he died.

“I’ve led an interesting life, but I can’t tell you what I’d give to be the guy you didn’t know anything about,” Sizemore wrote in his memoir.

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https://www.youtube.com/watch?v=RclTx0jcpMU

Even before ‘Ryan’ … Sizemore had already racked up several notable roles in flicks like “Where Sleeping Dogs Lie“, “Passenger 57“, “True Romance“, “Natural Born Killers“, “Devil in a Blue Dress“, “Heat,” “Enemy of the State” and lots of others. By this point, he’d carved out a nice little archetype for himself, often playing a tough guy and/or a hardened criminal.

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Tom Sizemore, ‘Saving Private Ryan’ actor, dies at 61

BURBANK, Calif. (AP) — Tom Sizemore, the “Saving Private Ryan” actor whose bright 1990s star burned out under the weight of his own domestic violence and drug convictions, died Friday at age 61.

The actor had suffered a brain aneurysm on Feb. 18 at his home in Los Angeles. He died in his sleep Friday at a hospital in Burbank, California, his manager Charles Lago said.

Sizemore became a star with acclaimed appearances in “Natural Born Killers” and the cult-classic crime thriller “Heat.” But serious substance dependency, abuse allegations and multiple run-ins with the law devastated his career, left him homeless and sent him to jail.

As the global #MeToo movement wave crested in late 2017, Sizemore was also accused of groping an 11-year-old Utah girl on set in 2003. He called the allegations “highly disturbing,” saying he would never inappropriately touch a child. Charges were not filed.

Despite the raft of legal trouble, Sizemore had scores of steady film and television credits — though his career never regained its onetime momentum. Aside from “Black Hawk Down” and “Pearl Harbor,” most of his 21st century roles came in low-budget, little-seen productions where he continued to play the gruff, tough guys he became famous for portraying.

I was a guy who’d come from very little and risen to the top. I’d had the multimillion-dollar house, the Porsche, the restaurant I partially owned with Robert De Niro,” the Detroit-born Sizemore wrote in his 2013 memoir, “By Some Miracle I Made It Out of There.” “And now I had absolutely nothing.

The book’s title was taken from a line uttered by his character in “Saving Private Ryan,” a role for which he garnered Oscar buzz. But he wrote that success turned him into a “spoiled movie star,” an “arrogant fool” and eventually “a hope-to-die addict.”

He racked up a string of domestic violence arrests. Sizemore was married once, to actor Maeve Quinlan, and was arrested on suspicion of beating her in 1997. While the charges were dropped, the couple divorced in 1999.

Sizemore was convicted of abusing ex-girlfriend Heidi Fleiss in 2003 — the same year he pleaded no contest and avoided trial in a separate abuse case — and sentenced to jail. The former Hollywood madam testified that he had punched her in the jaw at a Beverly Hills hotel, and beaten her in New York to the point where they couldn’t attend the “Black Hawk Down” premiere.

The sentencing judge said drug abuse was likely a catalyst but that testimony had revealed a man who had deep problems dealing with women. Fleiss called Sizemore “a zero” in a conversation with The Associated Press after his conviction.

The CDC says the ‘safety signal’ wasn’t seen in the Moderna COVID-19 vaccine

By Adam Sabes | Fox News

The Centers for Disease Control and Prevention (CDC) says that a preliminary COVID-19 vaccine “safety signal” has been identified and is investigating whether the Bivalent Pfizer-BioNTech vaccine creates an increased risk of ischemic stroke in people 65 and older.

In the Friday statement, the CDC said that the preliminary signal hasn’t been identified with the Bivalent Moderna COVID-19 vaccine.

“Following the availability and use of the updated (bivalent) COVID-19 vaccines, CDC’s Vaccine Safety Datalink (VSD), a near real-time surveillance system, met the statistical criteria to prompt additional investigation into whether there was a safety concern for ischemic stroke in people ages 65 and older who received the Pfizer-BioNTech COVID-19 Vaccine, Bivalent,” the CDC said.

According to the CDC, an ischemic stroke “occurs when blood clots or other particles block the blood vessels to the brain.”

In the statement, the CDC pointed out that a large study of updated bivalent vaccines from Pfizer-BioNTech “using the Centers for Medicare and Medicaid Services database revealed no increased risk of ischemic stroke.”

The agency also said that the Vaccine Adverse Event Reporting System (VAERS) managed by CDC and FDA has not seen an increase in reporting of ischemic strokes following the updated (bivalent) vaccine.

In a statement to Fox News Digital, a spokesperson for Pfizer said, “Pfizer and BioNTech have been made aware of limited reports of ischemic stroke that have been observed in the CDC Vaccine Safety DataLink (VSD) database in people 65 and older following vaccination with the Omicron BA.4/BA.5-adapted bivalent COVID-19 Vaccine by Pfizer and BioNTech.”

Liesl Eibschutz, a medical student from Dartmouth University, loads a syringe with Pfizer COVID-19 vaccine before giving it to people on the first day that people ages 16 and up can receive the vaccine at Kedren Health in Los Angeles on April 15, 2021. ( Allen J. Schaben / Los Angeles Times via Getty Images)

“Neither Pfizer and BioNTech nor the CDC or the U.S. Food and Drug Administration (FDA) have observed similar findings across numerous other monitoring systems in the U.S. and globally and there is no evidence to conclude that ischemic stroke is associated with the use of the companies’ COVID-19 vaccines,” the spokesperson continued.

“Compared to published incidence rates of ischemic stroke in this older population, the companies to date have observed a lower number of reported ischemic strokes following the vaccination with the Omicron BA.4/BA.5-adapted bivalent vaccine. The CDC continues to recommend vaccination with the Pfizer-BioNTech Omicron BA.4/BA.5-adapted bivalent COVID-19 vaccine for all authorized ages and indications.”

This August 2022 photo shows vials of Pfizer’s updated COVID-19 vaccine during production in Kalamazoo, Michigan.  (Pfizer via AP)

The CDC isn’t recommending a change in vaccine practice.

Fox News medical contributor Dr. Marc Siegel said that this isn’t “proof” of a link between the vaccine and strokes.

“This is not proof. This is that they see there may be a link here, and they want to investigate it, and they’re trying to be transparent,” he said.

CDC & FDA Identify Preliminary COVID-19 Vaccine Safety Signal for Persons Aged 65 Years and Older

source CDC

Transparency and vaccine safety are top priorities for the Centers for Disease Control and Prevention (CDC) and the Food and Drug Administration (FDA). U.S. government agencies use multiple, complementary safety monitoring systems to help detect possible safety signals for vaccines and other medical countermeasures as early as possible and to facilitate further investigation, as appropriate. Often these safety systems detect signals that could be due to factors other than the vaccine itself.

All signals require further investigation and confirmation from formal epidemiologic studies. When one system detects a signal, the other safety monitoring systems are checked to validate whether the signal represents an actual concern with the vaccine or if it can be determined to be of no clinical relevance.

Following the availability and use of the updated (bivalent) COVID-19 vaccines, CDC’s Vaccine Safety Datalink (VSD), a near real-time surveillance system, met the statistical criteria to prompt additional investigation into whether there was a safety concern for ischemic stroke in people ages 65 and older who received the Pfizer-BioNTech COVID-19 Vaccine, Bivalent. Rapid-response investigation of the signal in the VSD raised a question of whether people 65 and older who have received the Pfizer-BioNTech COVID-19 Vaccine, Bivalent were more likely to have an ischemic stroke in the 21 days following vaccination compared with days 22-42 following vaccination.

This preliminary signal has not been identified with the Moderna COVID-19 Vaccine, Bivalent. There also may be other confounding factors contributing to the signal identified in the VSD that merit further investigation. Furthermore, it is important to note that, to date, no other safety systems have shown a similar signal and multiple subsequent analyses have not validated this signal:

• A large study of updated (bivalent) vaccines (from Pfizer-BioNTech and Moderna) using the Centers for Medicare and Medicaid Services database revealed no increased risk of ischemic stroke
• A preliminary study using the Veterans Affairs database did not indicate an increased risk of ischemic stroke following an updated (bivalent) vaccine
• The Vaccine Adverse Event Reporting System (VAERS) managed by CDC and FDA has not seen an increase in reporting of ischemic strokes following the updated (bivalent) vaccine
• Pfizer-BioNTech’s global safety database has not indicated a signal for ischemic stroke with the updated (bivalent) vaccine
• Other countries have not observed an increased risk for ischemic stroke with updated (bivalent) vaccines

Although the totality of the data currently suggests that it is very unlikely that the signal in VSD represents a true clinical risk, we believe it is important to share this information with the public, as we have in the past, when one of our safety monitoring systems detects a signal. CDC and FDA will continue to evaluate additional data from these and other vaccine safety systems. These data and additional analyses will be discussed at the upcoming January 26 meeting of the FDA’s Vaccines and Related Biological Products Advisory Committee.

No change in vaccination practice is recommended. CDC continues to recommend that everyone ages 6 months of age and older stay up-to-date with COVID-19 vaccination; this includes individuals who are currently eligible to receive an updated (bivalent) vaccine. Staying up-to-date with vaccines is the most effective tool we have for reducing death, hospitalization, and severe disease from COVID-19, as has now been demonstrated in multiple studies conducted in the United States and other countries:

• Data have shown an updated COVID-19 vaccine reduces the risk of hospitalization from COVID-19 by nearly 3-fold compared to those who were previously vaccinated but have not yet received the updated vaccine.
• Data have shown that the updated COVID-19 vaccine also reduces the risk of death from COVID-19 by nearly 19-fold compared to those who are unvaccinated.
• Other preliminary data from outside the U.S. have demonstrated more than 80% protection against severe disease and death from the bivalent vaccine compared to those who have not received the bivalent vaccine.

Overall safety data for the bivalent COVID-19 vaccines are available here.

A Systematic Review and Meta-analysis

• Received February 4, 2022.
• Accepted in final form June 8, 2022.

• © 2022 American Academy of Neurology

Maria-Ioanna Stefanou, Lina Palaiodimou,  View ORCID ProfileDiana Aguiar de Sousa, Aikaterini Theodorou, Eleni Bakola,  View ORCID ProfileDimitrios Eleftherios Katsaros, Panagiotis Halvatsiotis, Elias Tzavellas, Androniki Naska,  View ORCID ProfileJonathan M. Coutinho, Else Charlotte Sandset, Evangelos J. Giamarellos-Bourboulis, Georgios Tsivgoulis source

Everyhting about – The COVID Vaccination read here

find out more directly from the company medication site www.activase.com

A protein that may hinder the brain’s regrowth after damage points researchers to an unexpected treatment

Stroke treatment has been a race against time. In the hours after a stroke, the clot-busting treatment tissue plasminogen activator (tPA) can limit damage to the brain. But once that damage is done, no drugs are known to promote recovery. New research suggests such a therapy could come from an unlikely target: a cellular protein called CCR5 that allows HIV to infect cells. Scientists found that in mice, disabling CCR5 helps surviving neurons make new connections, and that people who carry a CCR5 mutation may recover better from a stroke.

“This is the first real molecular target to improve recovery after stroke,” says Argye Hillis, a stroke neurologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, who was not involved in the work. A clinical trial will soon test its promise by giving stroke patients an HIV drug that blocks CCR5.

White blood cells display CCR5 on their surface to intercept signals from molecules called chemokines and coordinate an immune response. But HIV exploits CCR5, grabbing onto it to invade host cells. People with a mutation that cripples the CCR5 gene are protected from infection, which is why Chinese scientist He Jiankui recently aimed to mutate CCR5 in controversial human experiments.

The new discoveries about CCR5 began with a hunt for “smart mice”—animals bearing genetic mutations that apparently boost their ability to learn and remember. Neuroscientist Alcino Silva and his team at the University of California, Los Angeles (UCLA), wanted to figure out which of 148 mouse strains had such enhancements. In 2016, they reported that reducing levels of CCR5 in a healthy mouse brain enhanced memory formation and learning.

UCLA stroke neurologist Thomas Carmichael was intrigued. “When you watch patients recover in stroke, it looks like they’re relearning to walk or relearning language,” he says. Indeed, surviving neurons near the injury sprout tendrils to make new contacts across the brain. A drug that targets CCR5 seemed promising for stroke recovery, and that drug was already on hand. Maraviroc, which blocks CCR5, was approved by U.S. regulators in 2007 for use with other antiretroviral drugs to treat HIV infections.

In Cell this week, Silva, Carmichael, and their collaborators showed that CCR5 levels in mouse neurons skyrocket after stroke and can remain elevated for weeks—and that the protein appears to hamper recovery. The team blocked CCR5 with maraviroc or a gene that interferes with its production, and then ran the mice through tests of motor ability—for example, counting how many times their feet slipped as they walked across a metal grid. Treated mice showed greater motor improvements than controls at the end of the 9-week testing period.

Even if the researchers waited until 3 weeks after a stroke to give the animals maraviroc, it improved their performance. In previous studies, nothing has seemed to help at that point, says Dale Corbett, a neuroscientist specializing in stroke recovery at the University of Ottawa. The new results, he says, suggest “it may be feasible to reopen this recovery window in people.”

Blocking CCR5 seemed to help maintain connections between neurons adjacent to the injured site. And it caused neurons in motor regions to sprout more projections to the opposite side of the brain, a process that might help a mouse relearn lost movements.

What CCR5 does in the poststroke brain is hazy. Surging CCR5 is part of the inflammatory response to stroke, says Robyn Klein, a neuroimmunologist at Washington University School of Medicine in St. Louis, Missouri. In flammatory molecules may prompt neurons to express more of this chemokine receptor. In the developing brain, chemokines are known to influence how neurons migrate and connect. After stroke, they seem to decrease the number of connection sites on neurons near the damage. (How that process hinders regrowth and recovery isn’t clear.)

Carmichael notes that blocking CCR5 also caused neurons to express genes that increase their excitability, making them fire more readily. He suspects that neurons boost CCR5 after a stroke to dampen their activity and lie low to avoid a deadly cellular frenzy known as excitotoxicity. But because the protein then sticks around, that protective mechanism gets in the way of recovery.

Mouse results often prove meaningless in people, but when Carmichael’s group teamed up with researchers behind the Tel Aviv Brain Acute Stroke Cohort (TABASCO) in Israel, they found encouraging clues. Roughly 10% of Europeans have a genetic deletion that cripples CCR5, and the number is higher in Jewish people of Eastern European origin. The TABASCO team identified 68 people in its cohort of stroke survivors who had at least one copy of the CCR5 mutation. Compared with people without the mutation, they performed slightly better on tests of motor and sensory skills and cognitive abilities both 6 months and 1 year after a stroke, the new study found.

“It wasn’t gangbusters better, but … the fact that they found anything is impressive,” says Steven Cramer, a stroke neurologist at UC Irvine, who has studied genes linked to stroke recovery.

Carmichael and his collaborators are now designing a clinical trial that will give 30 people maraviroc starting when they leave an inpatient rehabilitation facility—typically about 4 weeks after a stroke. The team hopes to launch the trial this year.

Meanwhile, some researchers expect the CCR5 story to inspire a broader search for brain repair strategies based on learning and memory genes. “We’ve always been talking about having a tPA-like moment for stroke recovery,” Corbett says. “Whether this is it or not, I don’t know, but at least it gives us hope.”

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How are a stroke and heart attack different?

stroke vs. heart attack

Heart attack symptoms

Learning the warning signs of heart attack and stroke is important. Seek emergency medical care immediately if any symptoms appear.

Chest pain is one of most recognizable symptoms of a heart attack. While it is the most common symptom, many people who experience a heart attack have little to no chest pain.

These people may not realize that they are having a heart attack, and they may not seek medical care as quickly as needed.

Other symptoms that may indicate a heart attack include:

• a feeling of pressure, fullness, or squeezing in the chest
• pain in the jaw, neck, arms, back, or stomach
• feeling short of breath
• lightheadedness or fainting
• cold sweats
• nausea or vomiting

Women are more likelyTrusted Source than men to experience nausea, vomiting, shortness of breath, and jaw pain during a heart attack.

Anyone who experiences these symptoms should seek care immediately.

Stroke symptoms

There are two types of stroke: ischemic and hemorrhagic. Most people who have a stroke have an ischemic stroke. A blood clot in one of the brain’s blood vessels usually causes this.

A blockage or plaque does not cause hemorrhagic stroke. Instead, a burst artery can lead to this type of stroke.

A stroke can rapidly damage the brain, leading to permanent disability or death. Stroke symptoms begin quickly, often with no warning.

They may include:

• drooping on one side of the face, or being unable to move one side of the face
• weakness or numbness in one arm, in which the person may be unable to raise both arms evenly out to the side
• slurred speech or difficulty talking, during which the person may not be able to repeat simple words or sentences clearly
• vision loss in one eye
• loss of balance, frequent falling, or dizziness

A transient ischemic attack (TIA), or mini-stroke, produces symptoms very similar to a stroke, but it only lasts for a few minutes. A TIA does not permanently damage the brain.

However, do not ignore them. Around 4 in 10 people who have a TIA will go on to have a stroke.

Anyone who experiences stroke symptoms should see a doctor immediately, even if they pass quickly.

 

Causes

Atherosclerosis causes a buildup of plaque, a substance that restricts and hardens the blood vessels. This disease causes the majority of strokes and heart attacks.

Over time, the plaque can harden and break off, causing a blood clot to form. The clot can block the blood vessel and starve vital organs of oxygen.

During most heart attacks, a clot blocks a coronary artery, which is one of the heart’s blood vessels. Therefore, part of the heart muscle rapidly loses its blood supply and may incur permanent damage.

Similarly, most strokes are due to the blockage of a blood vessel somewhere in the brain. The clot robs the brain of its vital blood supply and can lead to brain damage.

Treatment

Blocked arteries and blood clots can cause both heart attacks and strokes. So, their treatment may be similar in several ways.

In both conditions, a doctor may prescribe a person clot-busting medicines in the hospital. These medications are called thrombolytics, and they help dissolve the blood clot and restore blood flow to the affected organ.

Doctors usually need to administer thrombolytics as soon as possible after the symptoms begin, or at least within a few hours of onset.

Through an endovascular procedure, a specialist may also physically remove any blood clots in the coronary or carotid arteries. This is a nonsurgical procedure that uses a thin tube to grip the clot and remove it.

Examples of an endovascular procedure include:

• percutaneous coronary intervention for heart attack
• mechanical thrombectomy for stroke

Not everyone would benefit from a clot-removing procedure after a stroke or heart attack. If this surgery takes place, a specialist should perform it as soon as possible after symptoms become apparent.

Recovery

After stroke or heart attack, doctors tend to prescribe certain medicines. These drugs can help by:

• reducing future plaque buildup in the arteries
• lowering blood pressure or cholesterol
• reducing blood clots

Taking these medicines long-term may help a person prevent another heart attack or stroke.

Though some heart attack and stroke medicines may overlap, different treatments can help each condition. A doctor will base the particular medications they prescribe on a person’s medical history.

People who have had a heart attack might receive specific medicines that can help reduce stress on the heart, prevent further heart damage, and relieve chest pain.

People who have diabetes have higher risk of stroke, so a doctor might choose to prescribe medications to help regulate blood sugar to control this increased risk.

Many cases of stroke and heart attack are due to plaque buildup inside the arteries. For this reason, either condition may involve certain lifestyle changes, including:

• following a heart-healthy diet
• getting regular exercise
• quitting smoking
• maintaining a healthy weight

These changes can help the body recover from a stroke or heart attack and reduce the risk of having another, as well as promote general wellness.

The most important factor of good recovery from a heart attack or stroke is getting treatment as soon as possible.

Differences in therapy

Recovery from many heart attacks and strokes requires some kind of rehabilitation or physical therapy. The type of therapy and the goals of the treatment are usually quite different between the two conditions.

Therapy following a heart attack

After a heart attack, a person may require cardiac rehabilitation.

This is specialized therapy designed to improve heart health. A doctor supervises this treatment.

Cardiac rehabilitation usually includes:

• Exercising: A cardiac rehabilitation specialist guides a person through exercise that is heart-healthy and safe for them to do.
• Receiving information about living a heart-healthy life: This includes adopting a healthful diet, quitting smoking, and managing heart attack risk factors.
• Reducing stress: Finding ways to manage stress can help improve heart health.

Therapy following a stroke

Therapy after a stroke is quite different from rehabilitation after a heart attack.

If a person experiences brain damage during a stroke, therapy might include a variety of exercises to help a person regain physical and psychological functions they may have lost.

Most strokes cause one of the following disabilities, which may be temporary or permanent:

• problems with movement or paralysis in certain areas of the body
• trouble swallowing
• changes in behavior or emotions
• problems with thinking and memory
• trouble talking or understanding other people
• uncontrolled urine leakage or bowel movements
• changes to vision, taste, or smell

Heart attack and stroke are similar in many ways, but each requires different care and follow-up.

Having a heart-healthy lifestyle and regularly visiting the doctor can help minimize the risk of these life-threatening conditions. However, it cannot prevent them entirely.

Q:  How are heart attack and stroke different from heart failure?

A:  Heart attack and stroke are both acute conditions, while heart failure is a chronic condition. Heart attack occurs when blood flow to part of the heart is blocked, causing an insult to the heart muscle. Stroke, on the other hand, occurs when blood flow from part of the brain is cut off due to a blocked or ruptured blood vessel.

Medical professionals consider heart failure a progressive and chronic condition. With heart failure, the heart cannot pump enough blood effectively to meet the demands of the body.

Gerhard Whitworth, RNTrusted Source Answers represent the opinions of our medical experts. All content is strictly informational and should not be considered medical advice.

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Induced Immune Thrombotic Thrombocytopenia

Abstract

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has infected 1 in 50 world citizens and claimed the lives of over 3 million people since December 2019.¹ Patients with severe coronavirus disease 2019 (COVID-19) are at high risk of thrombotic complications, with observational studies indicating up to one-third hospitalized with COVID-19 develop acute myocardial injury,² 15% to 30% develop venous thromboembolism (VTE),³ and 1% to 5% experience acute stroke.^4–7 It is because of these systemic complications that the mortality rate is 3× that of other viral infections such as seasonal influenza.⁸

The emergence of SARS-CoV-2 variants has been even more concerning.⁹ The B.1.1.7 variant, which originated in the United Kingdom, is reported to be more contagious than the original virus described in Wuhan,¹⁰ whereas both the B.1.1.7 and B.1.351 variants may be responsible for the lower efficacy of several current vaccines.^11–13 A global resurgence in case numbers since February 2021 may be explained by these emerging variants and leniency in public health measures.

At present, 5 vaccines are authorized for emergency use due to proven efficacy in clinical trials^14–19 (Table 1). Although randomized trials including >60 000 blinded vaccine recipients have demonstrated a low risk of serious adverse events, reports have emerged of rare thrombotic complications with 2 vaccines. In this commentary, we summarize the known risks of these vaccines compared with the known thrombotic and systemic risks of COVID-19.

Thrombosis in COVID-19

The thrombotic complications of COVID-19 have been well described.^3,4,20,21 As in patients without COVID-19, therapeutic anticoagulation is recommended in patients who develop VTE with COVID-19; however, there is no strong evidence to support the empirical use of therapeutic anticoagulation in unaffected persons.²² The ACTIV-4 trial (Anti-Thrombotics for Adults Hospitalized With COVID-19) comparing therapeutic against prophylactic anticoagulation based on d-dimer level halted enrollment of critically ill patients due to a signal for harm in patients randomized to therapeutic anticoagulation.²³ Preliminary data from the REMAP-CAP trial (Randomized, Embedded, Multifactorial Adaptive Platform Trial for Community-Acquired Pneumonia) suggested futility of therapeutic anticoagulation in critically ill patients with COVID-19.²⁴

Among locations for arterial and venous thrombosis in COVID-19, several reports^25–27 and a systematic review²⁸ have indicated a small but significant risk of cerebral vein thrombosis (CVT). It is estimated that COVID-19 increases the odds of CVT by >40-fold, affecting as many as 1 in 5000 to 15 000 hospitalized patients with COVID-19,^4,29 although the true prevalence among patients with COVID-19 is unknown. More than two-thirds of patients with COVID-19 with CVT lack traditional risk factors,²⁸ with a mortality rate greater than patients without COVID-19 with CVT.^28,29

CVT Associated With Adenoviral COVID-19 Vaccines

Early Reports and Event Rates

Since the approval of COVID-19 vaccines in December 2020 by the Food and Drug Administration and European Medicines Agency (EMA), >116 million vaccine sdoses have been administered in Europe and over 215 million doses in the United States, correlating with a significant decline in new case rates and fatalities from COVID-19 (Figure 1).

 

In February 2021, reports emerged of patients with thrombocytopenia and VTE in unusual locations following the ChAdOx1 vaccine, resulting in its suspension in several countries by mid-March. By April 4, 2021, 169 cases of CVT and 53 cases of splanchnic vein thrombosis were reported to the EMA among 35 ChAdOx1 million vaccine recipients.³⁰ On May 5, 2021, a population cohort study in Denmark and Norway reported increased rates of venous thromboembolic events, including CVT, among recipients of the ChAdOx1 vaccine with no increase in arterial events.³¹ These recent data suggest an excess event rate of CVT of 2.5 per 100 000 ChAdOx1 recipients, although laboratory testing has not confirmed that these events are due to vaccine-induced immune thrombotic thrombocytopenia (VITT).

In the United States, 17 recipients of Ad26.COV2.S (of 7.98 million recipients) were found to develop CVT and thrombocytopenia, with 14 cases of CVT (3 of which were fatal),³² leading the Centers for Disease Control (CDC) and EMA to recommend temporary discontinuation of this vaccine. Twelve of these patients have been described in detail by See et al.³³ We have summarized the patient-level data for reported individuals in Table I in the Data Supplement.^33–41 Importantly, the majority of decedents were middle-aged or older (median age 69 years, range 21–97), also indicating a low risk of dying from the vaccine among younger recipients.³²

The unique presentation of these thrombotic events with thrombocytopenia and the temporal relationship with vaccination has been termed VITT. As more cases have been reported to the EMA and CDC, the estimated incidence of VITT is ≈1 in 150 000 for the ChAdOx1 nCov-19 vaccine and 1 in 470 000 for the Ad26.COV2.S vaccine (Figure 2), although the risks may vary per age group and sex. Although these events may be increasingly recognized, the absolute numbers are small and the epidemiological data continue to overwhelmingly support the safety and efficacy with respect to COVID-19 risk reduction and death due to COVID-19 (or vaccines) among vaccine recipients irrespective of age (Table 2).^15,19,32,42

Pathophysiology

Cases of VITT have not been reported following other adenovirus-based vaccines or mRNA-based COVID-19 vaccines. Although adenoviruses are known to activate platelets, it is unlikely that the thrombocytopenia following vaccination is due to the adenoviral vector.¹⁵ Additionally, there have been no reported cases of VITT following administration of either the other adenoviral coronavirus vaccines (AD5-nCOV or Gam-COVID-Vac) or adenovirus-based Ebola virus vaccines (Ad5-EBOV and Ad26.ZEBOV).⁴³

The association of unusual thrombotic complications with thrombocytopenia raised suspicion for inflammatory coagulopathy. Investigators identified antibodies targeting PF4 (platelet factor 4) in the sera of patients with VITT,³⁵ suggesting an autoimmune vaccine response. A similar mechanism has been described in heparin-induced thrombotic thrombocytopenia (HITT; Figure 2).⁴⁴ In HITT, antibodies are directed against PF4 (found on platelets and the vascular endothelium) complexed with heparin. Once this complex forms, the Fc region on the platelet is captured by the Fc region on adjacent platelets, perpetuating platelet aggregation.⁴⁵ Thrombocytopenia occurs when IgG-coated platelets are removed by the reticuloendothelial system and consumed at sites of thrombosis.⁴⁶

The time from vaccine to symptom onset is 5 to 16 days following the ChAdOx1 vaccine.^35,36 Patients had no previous exposure to heparin, suggesting that the anti-PF4 (antibodies directed against platelet factor 4) are a novel humoral response to the vaccine. One possible explanation may be the complexing of nucleic acid contained in the vaccine to PF4.³⁵ Importantly, the incidence rate of VTE as part of this idiosyncratic response to coronavirus vaccines remains low, with extremely rare thrombosis occurring in the cortical veins and dural sinuses (Figure 2). The novelty of this discovery suggests these events may be more common than reported (Figure 3).

Figure 3. Annualized incidence rates for cerebral vein thrombosis (CVT). COVID-19 indicates coronavirus disease 2019.

Diagnostic Evaluation of CVT and VITT

A high index of suspicion is important in the detection of CVT with VITT for patients who present within 4 weeks of adenovirus-mediated vaccination. In patients with new severe headache, subacute encephalopathy, visual loss, seizure, or focal neurological deficit, a complete blood count and head computed tomography with venography with or without angiography or magnetic resonance imaging with a venogram is recommended.⁴⁷ If either the platelet count is <150 000/µL or the neuroimaging is suggestive of CVT, the patient will be tested for anti-PF4, preferably an anti-PF4 ELISA.⁴⁸ Patients with thrombocytopenia should be verified for platelet clumping and recent heparin exposure as alternative mechanisms to explain the low platelets.

Empirical treatment should not be delayed while results are pending. Consultation with a physician with expertise in thrombosis is recommended by the American Heart Association/American Stroke Association to assist in antithrombotic selection and management of CVT⁴⁹ (with or without VITT) and may aid in the evaluation for alternative causes of consumptive thrombocytopenia. We recommend testing for SARS-CoV-2 by nasopharyngeal polymerase chain reaction, as present vaccines are not fully protective against viral infection, and as COVID-19 has been associated with a low but significant risk of CVT.²⁵ Other causes and risk factors of CVT ought to be considered (Figure 4).⁵⁰

Management of CVT With VITT

Given the similar mechanism of anti-PF4–induced platelet activation between VITT and HITT, experts recommend that treatment of VITT parallels the treatment of HITT (Figure 4).⁴⁷

Figure 4. Management of vaccine-induced immune thrombotic thrombocytopenia (VITT). Note that the 1 in 40 000 risk of cerebral vein thrombosis (CVT) following ChAdOx1 vaccination is derived from the estimate by Pottegård et al³¹ regarding excess event rates rather than laboratory confirmed VITT in CVT. For these excess events, VITT should be suspected. Image generated using Biorender.com. COVID-19 indicates coronavirus disease 2019; CTV, computed tomography venogram; HITT heparin-induced thrombotic thrombocytopenia; MRV magnetic resonance venogram; PF4 platelet factor 4, IVIg intravenous immunoglobulin; and VTE, venous thromboembolism.

Pharmacological Intervention for Presumed VITT

Empirical interventions should target both the autoimmune and thrombotic sequela. As platelet activation via autoantibody formation is thought to be the principal mediator of thrombosis, IVIg (intravenous immunoglobulin) 1g/kg daily for 2 days is recommended,³⁷ although the 2018 Guidelines from the American Society of Hematology do not support its routine use in the related HITT syndrome.⁵¹ Potential adverse effects from IVIg including headache, flushing, and aseptic meningitis should be weighed with its potential benefits. High-dose corticosteroids, plasma exchange, and fibrinogen substitution may be considered for severe thrombocytopenia.⁵²

Although there is no evidence that administering heparin for CVT related to VITT is harmful, nonheparin-based intravenous anticoagulants (argatroban, bivalirudin, fondaparinux) are considered due to the presence of anti-PF4 antibodies and overlapping mechanisms with HITT. Oral anticoagulants (rivaroxaban, apixaban, dabigatran) may be considered after clinical stabilization. Anticoagulation with a direct oral anticoagulant or with a vitamin K antagonist should continue for 3 to 6 months or until radiographic resolution of the CVT.⁴⁹ The American Heart Association/American Stroke Association guidelines recommend anticoagulation be initiated or continued in the presence of hemorrhagic venous congestion,⁴⁹ although this remains debated.⁵³ In these cases, the associated edema and hematoma size may warrant decompressive hemicraniectomy or hematoma evacuation to prevent fatal herniation. Alternatively, such patients might benefit from endovascular thrombectomy.

Platelet transfusions are not recommended for thrombocytopenia in VITT^37,48 unless a life-threatening hemorrhage is present,⁴⁸ as in HITT guidelines.⁵¹ Furthermore, due to the unique mechanism of intracranial hemorrhage in CVT from venous congestion, CVT-associated hemorrhage is unlikely to stabilize with platelet transfusion. Restoration of venous outflow in the form of therapeutic anticoagulation or endovascular intervention is critical to reduce local venous congestion and intracranial pressure, which may prevent edema formation and hematoma expansion.

It is unclear, but heparin (unfractionated and low-molecular weight heparin) may worsen symptoms of VITT due to the mechanistic overlap with HITT. Between 2 previously published series of VITT,^35,36 heparin was administered to 11 of 16 patients, with 5 early fatalities. Based on limited data, it is unclear if this mortality rate represents the natural history of the condition or if it reflects a complication of traditional interventions for venous thrombosis. That said, increasing platelet counts were observed in these patients who received concomitant prednisolone and IVIg without evidence of recurrent or increased thrombosis.

Endovascular Retrieval

In patients with deteriorating mental status, endovascular thrombectomy can be considered according to American Heart Association/American Stroke Association guidelines (Class IIb, Level of Evidence C).^49,54 However, the benefit of thrombectomy in CVT over medical management was not demonstrated in the recent TO-ACT randomized clinical trial (Thrombolysis or Anticoagulation for Cerebral Venous Thrombosis).⁵⁵ Because TO-ACT terminated early due to futility, it is possible that thrombectomy may benefit some patients with refractory CVT.

In a patient undergoing venous thrombectomy, if the patient is confirmed or suspected of having VITT, alternatives to heparinized saline flushes (eg, bivalirudin⁵⁶) may be considered.

COVID-19 Vaccine Paradigms and Challenges

Challenges exist in evaluating the risks and benefits of the continued use of the ChAdOx1 and Ad26.COV2.S vaccines. In cases of potentially life-threatening medical conditions, treatments that carry significant risks remain acceptable. Conversely, the risks involved in the prevention of a medical condition are far less tolerable. Vaccination against COVID-19 using these 2 vaccines carries the risk of a severe complication with a very low incidence (VITT). It is presently unknown what factors, if any, influence the risk of VITT. All vaccines currently being administered in the United States and Europe are available through emergency use decrees rather than through a typical approval process. Such decrees are granted based upon interim analysis of data that may not fully capture the side effect profiles of the intervention. In countries with widespread transmission of SARS-CoV-2, both the World Health Organization and the EMA have suggested that the benefits of vaccination far outweigh the risk of VITT. Shared decision-making and informing the patient of the very low risk of VITT are recommended to clinicians before administration of an adenovirus-based vaccination.

Use of the ChAdOx1 vaccine was resumed in many European countries on March 18, 2021, following a declaration by the EMA. Denmark announced on April 14, that the ChAdOx1 vaccine would not be used following 2 cases of VITT in 140 000 vaccinations. On April 20, 2021, Johnson & Johnson announced their intent to continue administering the Ad26.COV2.S vaccine in Europe following an EMA Pharmacovigilance Risk Assessment Committee report. On April 23, the CDC and Food and Drug Administration recommended the resumption of the Ad26.COV2.S vaccine in the United States based upon a favorable risk-benefit analysis.⁵⁷

A booster vaccine or annual inoculations may be needed to protect from COVID-19 and emerging variants. In patients who developed VITT from an adenovirus-mediated vaccine, we recommend switching to an mRNA-based vaccine if a second dose is needed.⁵⁸ In the absence of a VITT related event with the first vaccine, repeat immunization with the previous vaccine type is recommended by the CDC.⁵⁹

Gaps in Knowledge

The mechanism by which PF4 antibodies develop after adenovirus vaccine exposure remains unknown. It is not known whether VITT has a predilection for the cerebral venous sinuses or the splanchnic bed, compared with more common locations for VTE (such as lungs or legs). Based on population data, it is unknown why VITT has a predisposition for venous rather than arterial thromboembolism.³¹

Although a rare event, it is unclear why there is a skew towards this affliction in young women, although the United Kingdom VITT series reported 40% of patients were men, and the age extended to a patient in their seventies.³⁷ Predicting VITT will be challenging. In patients who are at higher risk for developing VTE (eg, family history, hypercoagulable state, oral contraceptives, prior VTE), it is not known whether they are at risk of developing VITT. However, when alternative vaccines may be available, a preferential strategy to offer these patients mRNA vaccines may be advised.

Conclusions

The consequences of the COVID-19 pandemic cannot be understated. Global health measures aimed at reducing the spread of the virus, including community education, universal masking, social distancing, and handwashing, have only temporized the pandemic. To date, the best treatment of COVID-19 involves supportive care and management of the para-infectious complications, including thrombotic events. The emergence of more contagious variants may accelerate the spread of the virus.

The optimal means of reducing the spread of SARS-CoV-2 remains mass pharmacological prophylaxis and establishment of herd immunity. The COVID-19 vaccines have proven efficacy against infection with SARS-CoV-2, severe COVID-19, and they have proven efficacy against emerging SARS-CoV-2 variants. Of the rarer complications of these vaccines, an autoimmune-mediated thrombotic thrombocytopenia is likely to be increasingly recognized. To date, this complication is unique to adenoviral coronavirus vaccines and preferentially affects young and middle-aged women without preexisting conditions. Early recognition, diagnosis, and treatment of VITT tailored to its pathophysiology (ie, suppressing the antibody response with IVIg, avoiding platelet transfusions, reducing thrombus burden with nonheparin-based anticoagulants) may improve the current high mortality rate of VITT (20%–30%).^32,58

Although the morbidity and mortality of VITT are highly concerning, it remains a rare event. The patient-level and societal benefits of vaccination vastly exceed the known risks of available coronavirus vaccines. We strongly encourage healthcare providers to continue recommending any available and approved COVID-19 vaccine for eligible persons because the risks of COVID-19 are greater than the risks of CVT. However, if >1 vaccine option is available, it may be reasonable to consider a nonadenoviral vaccine for women under the age of 50 years. In light of the United Kingdom VITT data,³⁷ it may be reasonable to extend consideration of nonadenoviral vaccines for young men as well. A high index of suspicion for VITT is important as early diagnosis can impact patient management and outcome.

As we learn more about VITT, recommendations for management are likely to change. It would be prudent to consult a local hematologist in the event of any suspicious event and apply updated guidance statements from the CDC, World Health Organization, or other hematologic society into the care of patients with this rare complication. Providers are reminded to report new cases to the Vaccine Adverse Event Reporting system (https://vaers.hhs.gov/) to better understand the true incidence of this entity and other complications.

Supplemental Materials

Online Table I

Footnotes

source: James E. Siegler,Piers Klein,Shadi Yaghi,Nicholas Vigilante,Mohamad Abdalkader,Jonathan M. Coutinho,Feras Abdul Khalek and Thanh N. Nguyen

Cerebral venous thrombosis after vaccination against COVID-19 in the UK: a multicentre cohort study

Summary

(A) Comparison of the outcomes from cerebral venous thrombosis in patients with VITT versus patients without VITT. (B) Comparison between VITT-associated cerebral venous thrombosis and historical data from the International Study on Cerebral Vein and Dural Sinus Thrombosis cohort. Each horizontal bar represents the percentage of patients in each modified Rankin scale category, which varies from 0 (no symptoms) through to 5 (severe disability). 6 represents death during this hospital admission. Diagonal lines and p values show comparisons of death and dependency (modified Rankin score 3–6) or death (modified Rankin score 6). VITT=vaccine-induced immune thrombotic thrombocytopenia.

The proportion of patients with VITT who had died or were dependent on others for their care at the end of admission was significantly lower in those given non-heparin parenteral anticoagulation (18 [36%] of 50 patients) compared with those who were not (15 [75%] of 20 patients; p=0·0031), in those who were given a direct oral anticoagulant (four [18%] of 22 patients) compared with those who were not (29 [60%] of 48 patients; p=0·0016), and in those who were given intravenous immunoglobulin (22 [40%] of 55 patients) compared with those who were not (11 [73%] of 15 patients; p=0·022; table 2).

Soruces

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• Richard J Perry, PhD  
• Arina Tamborska, MBChB
• Bhagteshwar Singh, MRCP
• Brian Craven, MBBCh
• Richard Marigold, FRCP
• Peter Arthur-Farraj, PhD

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