MESSAGE
| DATE | 2020-05-07 |
| FROM | Ruben Safir
|
| SUBJECT | Subject: [Hangout - NYLXS] Cadiac Events and Wuhan-19
|
https://news.harvard.edu/gazette/story/2020/04/covid-19s-consequences-for-the-heart/
COVID-19 may spark cardiac trouble in multiple ways
By Ekaterina Pesheva HMS Communications
DateApril 14, 2020
Email
Facebook
Twitter
LinkedIn
This is part of our Coronavirus Update series in which Harvard
specialists in epidemiology, infectious disease, economics, politics,
and other disciplines offer insights into what the latest developments
in the COVID-19 outbreak may bring.
Lung injury and acute respiratory distress syndrome have taken center
stage as the most dreaded complications of COVID-19, the disease caused
by the new coronavirus, SARS-CoV-2. But heart damage has recently
emerged as yet another grim outcome in the virus’s repertoire of
possible complications.
COVID-19 is a spectrum disease, spanning the gamut from barely
symptomatic infection to critical illness. Reassuringly, for the large
majority of individuals infected with the new coronavirus, the ailment
remains in the mild-to-moderate range.
Yet, a number of those infected develop heart-related problems either
out of the blue or as a complication of preexisting cardiac disease. A
report from the early days of the epidemic described the extent of
cardiac injury among 41 patients hospitalized with COVID-19 in Wuhan,
China: Five, or 12 percent, had signs of cardiovascular damage. These
patients had both elevated levels of cardiac troponin — a protein
released in the blood by the injured heart muscle — and abnormalities on
electrocardiograms and heart ultrasounds. Since then, other reports have
affirmed that cardiac injury can be part of coronavirus-induced harm.
Moreover, some reports detail clinical scenarios in which patients’
initial symptoms were cardiovascular rather than respiratory in nature.
How does the new coronavirus stoke cardiac damage?
The ways in which the new coronavirus provokes cardiac injury are
neither that new nor surprising, according to Harvard Medical School
physician-scientists Peter Libby and Paul Ridker. The part that remains
unclear is whether SARS-CoV-2 is somehow more virulent toward the heart
than other viruses. Libby and Ridker, who are practicing cardiologists
at Brigham and Women’s, say COVID-19-related heart injury could occur in
any several ways.
First, people with preexisting heart disease are at a greater risk for
severe cardiovascular and respiratory complications from COVID-19.
Similarly, research has shown that infection with the influenza virus
poses a more severe threat for people with heart disease than those
without cardiac problems. Research also shows that heart attacks can
actually be brought on by respiratory infections such as the flu.
Second, people with previously undiagnosed heart disease may be
presenting with previously silent cardiac symptoms unmasked by the viral
infection. In people with existing heart-vessel blockages, infection,
fever, and inflammation can destabilize previously asymptomatic fatty
plaques inside the heart vessels. Fever and inflammation also render the
blood more prone to clotting, while also interfering with the body’s
ability to dissolve clots — a one-two punch akin to throwing gasoline on
smoldering embers.
“It’s like one big stress test for the heart,” said Ridker, the Eugene
Braunwald Professor of Medicine at Brigham and Women’s Hospital.
Peter Libby and Paul Ridker.
Peter Libby (right) and Paul Ridker have been studying the potential
impacts of COVID-19 on the heart.
Photo courtesy of Harvard Medical School
Third, some people may experience heart damage that mimics heart attack
injury even if their arteries lack the fatty, calcified flow-limiting
blockages known to cause classic heart attacks. This scenario can occur
when the heart muscle is starved for oxygen, which in the case of
COVID-19 may be triggered by a mismatch between oxygen supply and oxygen
demand. Fever and inflammation accelerate heart rate and increase
metabolic demands on many organs, including the heart. That stress is
compounded if the lungs are infected and incapable of exchanging oxygen
and carbon dioxide optimally. This impaired gas exchange can further
diminish oxygen supply to the heart muscle.
Finally, there is a subset of people with COVID-19 — some of them
previously healthy and with no underlying cardiac problems — who develop
fulminant inflammation of the heart muscle as a result of the virus
directly infecting the heart. This type of inflammation could lead to
heart rhythm disturbances and cardiac muscle damage as well as interfere
with the heart’s ability to pump blood optimally.
The propensity of certain viruses to attack the heart muscle and cause
viral myocarditis is well known, Libby said, adding that the most
notorious viral offender has been the Coxsackie B virus. A recent case
report from Italy underscores the notion that the new coronavirus could
also infect the heart and affect heart muscle function in healthy adults
even after the acute phase of the infection has resolved and even in the
absence of lung damage.
“There are definitely some people who develop acute fulminant
myocarditis — in which the virus infects the heart muscle itself or the
cells within the heart — and causes a horrible inflammatory reaction,”
said Libby, the Mallinckrodt Professor of Medicine at Brigham and
Women’s Hospital. “This can be life threatening, and it can happen in
people who don’t have any preexisting risk factors.”
Libby and Ridker, however, say this out-of-the-blue scenario in
otherwise healthy individuals is likely rare relative to the overall
number of people with COVID-19 who experience heart problems.
The frenemy within
For Ridker and Libby, the cardiac involvement in COVID-19 is yet another
striking example of the widespread effects of inflammation on multiple
organs and systems. Inflammation is a critical defense response during
infection, but it has a dark side. Infections can set off a cascade of
immune signals that affect various organs.
Libby and Ridker hypothesize that any infection in the body — a
festering boil, an injured joint, a virus — can become a source of
inflammation that activates the release of inflammatory proteins known
as cytokines and calls up armies of white blood cells and other
messenger molecules that, in an effort to fight the infection, disrupt
normal processes. When these inflammatory molecules reach the welcoming
soil of a fatty deposit in the blood vessel wall — one that is already
studded with resident inflammatory white blood cells — the cytokines can
boost the local inflammatory response and trigger a heart attack.
“Our work has shown that cytokines can impinge on these cells in the
plaque and push it through a round of further activation,” Libby said.
“[Heart inflammation] can be life threatening, and it can happen in
people who don’t have any preexisting risk factors.”
— Peter Libby
The inflammatory chemicals released during infection can also induce the
liver to ramp up the production of important proteins that defend the
body from infection. These proteins, however, make the blood more prone
to clotting, while also reducing the secretion of natural
clot-dissolving substances. The tiny clots that may form can clog the
small blood vessels in the heart and other organs, such as the kidneys,
depriving them of oxygen and nutrients and setting the stage for the
multisystem failure that can occur in acute infection.
Thus, immune-mediated injury to the heart and other organs could be
collateral damage because of the body’s overwhelming systemic immune
response — a condition known as cytokine storm, which is marked by the
widespread release of cytokines that can cause cellular demise, tissue
injury and organ damage.
COVID-19 and blood pressure medications
SARS-CoV-2 invades human cells by latching its spike protein onto the
ACE2 receptor found on the surface of cells in the airways, lungs,
heart, kidneys and blood vessels. The ACE2 protein is an important
player in the renin-angiotensin-aldosterone system, which regulates
blood vessel dilation and blood pressure. Two classes of drugs widely
used to treat high blood pressure and heart disease — ACE inhibitors and
angiotensin receptor blockers — interact with the ACE2 receptor. A
possible concern related to COVID-19 stems from the notion that these
blood pressure medications could increase the number of ACE2 receptors
expressed on cells, possibly creating more molecular gates for the virus
to enter. Some experts have wondered whether the use of such drugs could
render people who take them more susceptible to infection. Conversely,
others have postulated that the abundance of ACE2 receptors may enhance
cardiovascular function, exercising a protective effect during infection.
The answer is far from clear, but a recent review suggests these
medicines may play a dual role in COVID-19 — on the one hand, enhancing
susceptibility to infection and, on the other, protecting the heart and
ameliorating lung damage from the disease.
Libby and Ridker cautioned that patients who take such life-saving
medications should stay on them or at least have a careful discussion
with their cardiologists. This is because these drugs have clear and
well-established benefits in hypertension and certain forms of heart
disease, while their propensity to make humans more susceptible to
SARS-CoV-2 remains speculative for the time being.
But what remains speculative today will crystalize in the weeks and
months to come, Ridker and Libby said, because the science is moving
forward rapidly, with new papers coming out daily and a growing pool of
patients to draw observations from.
Related
Ofer Levy an David Dowling.
Global race to a COVID-19 vaccine
Team at Harvard plans to launch clinical trial in fall
Giang Nguyen.
By phone and online, the care continues
Health Services director Giang Nguyen talks about adding remote services
and new resources for Harvard community
People walking 12 feet apart.
Hope for managing hospital admissions of COVID-19 cases
New projections suggest social-distancing measures in state may be
flattening the curve
“In 12 to 18 months we’re going to have a great deal of information, but
right now our job is to, number one, keep people from getting COVID-19
by strict adherence to now-familiar containment measures,” Libby said.
“Then, we need to get people who get the disease through this acute phase.”
The need for rigorous randomized trials done quickly and effectively is
acute, they said. Until the evidence from these trials begins to
coalesce, clinicians will have to navigate the uncharted territory of
delivering cardiac care in the time of pandemic with caution but also
with resolve.
“We don’t have the comfort of our usual databases, so we have to rely on
our clinical skills and judgment. But we have to do so in all humility
because often data don’t bear out our logical preconceptions,” Libby
said. “Yet, we must act.”
--
So many immigrant groups have swept through our town
that Brooklyn, like Atlantis, reaches mythological
proportions in the mind of the world - RI Safir 1998
http://www.mrbrklyn.com
DRM is THEFT - We are the STAKEHOLDERS - RI Safir 2002
http://www.nylxs.com - Leadership Development in Free Software
http://www.brooklyn-living.com
Being so tracked is for FARM ANIMALS and extermination camps,
but incompatible with living as a free human being. -RI Safir 2013
_______________________________________________
Hangout mailing list
Hangout-at-nylxs.com
http://lists.mrbrklyn.com/mailman/listinfo/hangout
|
|
