interaction friends cascini d'italia good evening free medicine answers
this evening with us is a welcome return that of doctor adriana
privacy welcome doctor and then obviously the top bolgar hello loretta
fabio we are doing around the co lead tonight we still face him from
another different perspective and which also concerns the right heart us and yes
exact so tonight we will talk about the complications
heart related to the co leader here so I would just like to ask the
In the meantime, doctor, you can get an overview of the course of the disease e
report just the cardiac complications
yes thanks then began with two definitions is the
definition of the heart is that it comes from the Latin cor cordis have
intelligence and at the Indo-European root from sky which means to vibrate and dance
this today expresses more than ever the characteristic of the heart a heart that
that is, it has a main action which is that of kompa ciliata
dress a little poor's like this while defining the
virus comes from the Latin poison toxin and from the Indo-European root vis active e
aggressive we will talk about the aggressiveness of the coronavirus virus
in particular by focusing on its aggressive action on
heart for a year now numerous studies have confirmed that a patient
who has heart disease definitely develops more
serious in this infection and therefore year in some ways can be said to be a prognosis
negative but why why probably a patient who has heart disease
also of the comorbidities that is of the concomitant diseases
diabetes is often of hypertension chronic renal failure age
advanced can also be a patient who has had a previous history in
made a heart disease of another type a patient who has had a
previous heart attack is also a situation of a heart that is not functioning
perfectly what is called heart failure but that is not necessarily the case
all patients must have had a heart attack
the coronavirus also affecting the vessels especially the coronaries can go
to determine obstructions we will see later why coronary arteries
resulting in a heart attack this percentage is 8-12 percent
it was found while 7 to 16 percent believed it in patients who have
section of the cords with the involvement of the heart an inflammation of the
heart cells as this information is called is called myocarditis
but not only is it an inflammation of the heart cells yes also a
inflammation of madness or that covers the heart this leaflet you must
imagining it as a film that surrounds the heart is called the pericardium
therefore we can have at a type myocarditis or pericarditis
even myocardial pericarditis so an inflammation of all is the structure
of the heart but the inflammation will also involve the coronary vessels which are i
vessels that supply the heart what we have seen we have unfortunately seen that in the
patients and who died of co leads and who had mostly
cardiac involvement therefore damage to the heart
the findings of anatomopathology highlight what show that the
heart cells which are called my ct appear as con cells
strong suffering therefore with necrotic parts then
fabric death and for parks instead of fabric which is as repaired
so we have areas of normal tissue of areas of necrotic tissue
on the other hand, one of the other scarring areas is a difference in the structure
of the tissue of the heart this is one of the reasons why i
patients who have heart involvement develop arrhythmias what
arrhythmias are themes which are irregular heartbeats
generally the arrhythmias that occur in these patients are arrhythmias
therefore severe ventricular arrhythmias which then degenerate into a rhythmic one
deadly and causing sudden death sudden death and 99.9
percent due to rhythmic such as ventricular fibrillation because yes
trigger because from the structure I have just described to you they can
check the circuits thus called re-entry circuits that arise
precisely of tachycardias because of the different from the different structure of the heart
in part normal tissue in part reparative tissue but there is also another
reason you can also trigger the zones of the members there is precisely from the points in
which the cells so inflamed adami meet abnormal beats that then
tachycardia comes out of it but in the case of myocarditis they can
be also inflammatory infiltrations and at the level of
of conduction where the stimulus is conducted that determines non-arrhythmias
pertinent and therefore not acceleration of the heartbeat of arrhythmias
hypokinetics for which atrioventricular blocks can also be found
then a series of arrhythmias from what comes out of how it detects that there is a
damage of the heart is detected by the specific markers which are the markers
specific markers that indicate heart damage precisely marks where
main is troponin is troponin always increases when we damage heart
and specifically for the heart then there are other markers in the
crosses that are the of you need to rome are less specific is your own than always
even in this case if I give you the heart
then when the virus enters and infects our cells we have to imagine
that enters through many doors and through things through the cavity
oropharyngeal can arrive in the intestine can arrive in the lung can
from the intestine because it is a profiteer I repeat it returns by infecting
bacteria and can induce viruses can infect the cells that are deputies
to our first defense that they are macrophages then vice po everywhere
what does it do because this is an RNA virus that transcribes in the cell nucleus
it lacks its rna and leads the cell to replicate other viruses
therefore the cell no longer replicates it is transformed no longer replicates its own
cell daughter cells but replicates what proteins am also sony vi
i will tell me how many mijoni are inside the cell are not active at some point
the cell breaks down and by breaking it puts these visions around
michela nigi you have to imagine them as signs that are thrown into a
ground so many seedlings are formed these whistles what are the mylius that
they go to infect other cells that is why disease does not disease
organ so therefore that it affects only the first stage
I would say about the virus infection which may be the intestine which may be his
lung especially the first b and sets in setting all the others
the other organs but as the virus arrives inside the cells it arrives
through a protein that I believe we all know by now may have
the first photo thanks here you see this is the image that I believe now that not between
all of them and where you can see these bad spikes these on tones
make up the spike protein this spike protein is what
allows the virus to enter the cell and is made up of 2 suffered by
s1 which binds to a cell gate called ace 2 receptor
and the others instead the suv an s2 protein is that binds the virus to the wall
mobile phone from the three photos thanks ok here you can see how the virus falls and the
baco the spike protein to enter proposes the ace 2 receptor
this age ii receptor is part of the renin angiotensin system than the other
photo thanks ok with the activation of the renin system
angiotensin and then transformation of angiotensin omino joe tehan up to
2 activates two receptors which are attimino and t2 which have two effects
completely different because the tv is mediated by the vague determines the plea
tation data a instead leads to vasoconstriction so this is a bit
the beginning pretty much how this virus enters
through that very little spike paddling in our cells
so then you can delve into the effect that sex as 2 has on hers
particular hill system the spike because this then leads to the consequences
important is alive to glimpse that at the level of load and cardiac here then
this we say that then the symptoms that are are very relevant
yes you can be a really new really interesting speech because you are
since it is the protein spain that the possibility of the spike protein in addition to
determine what I have described to you proto on tissue necrosis la
repair is also due to the increase in cytokines that take place gone
out ugly dani macrophages the first warriors the virus determines just one
inhibition of nascent scholine ie acetylcholine and new transmitter plus
It is important that we have the vagus nerve in the wide vagus located throughout the
body has the proper name of vague because vague is present in the whole body with è
its function therefore nice solution to release acetylcholine and of
but heart level cause a reduction in heart rate
because because the father is part of the slowing of the heartbeats
that start right from the sinoatrial node so acetylcholine is
this then also determines a stimulation of gastric motility
it creates a release that is really important to
narrowing of the pupils is an extremely important action for which i
I reconnect the breastfeeding 2 to dilation of the arteries and then when the salt
prodi ii inhibits acetylcholine which leads to an increase in
heart rate is a sometimes dramatic block of the gods urge mobile
from the gas system danger of the gastrointestinal system a very important
vasoconstriction because it acts on the two acts because they prevail at this point
on the two acts the acts 1 and therefore a very important vasoconstriction of the
artists or resulting in high blood pressure and hypertension that can
to reach even very high values ​​even 230 240 this inflamed tissue
as in the brain and such an important gap the question can
sometimes also cause cerebral hemorrhages but acetylcholine is part of it
also in a modulation also of the immune system through always the
vagus because we have seen the vagus nerve in the vicinity of the macrophages that are the
first intervening cells of our activated in our system
innate immune that intervenes immediately to try to fight this mini
course that is entering our body and our neighboring cells
of my own acetylcholine interacts with a particular community
what is called the 37 of the macrophages is that it involves a deactivation of the macro
choco but above all it inhibits the release of cytokines by the macrophage
one of the cytokines is more aggressive for our body for our defense
immune system is buzzing in the nose and therefore in fact that vague
nothing in the immune system we say that when we have the block and
acetylcholine we have an increase of what right there for inflammation
which is a feature of this of this disease
so this is a bit in summary, however, we remember that ours
motor system consists of an autonomous motor system that talks
phyto from the sympathetic and the motor system of the parasympathetic the mediator of the
parasympathetic through the vagus and sympathetic acetylcholine went there
adrenaline and noradrenaline while somatic motor system and what
it only checks the voluntary movements this more or less as a little idea
those like on our system of the question that they made me the
doctor and how the sar skovde two works so they are of the era effects
many important on the cig the choline which then become in our body then
also speech of the king ventricular cardiac athletes no what it can bring
just like I said before sudden death also linked to this a
this system correct and but therefore doctor with the increase of the frequency
but it is more related to what I said to the alteration of the structure
myocardial with cells with reparative cells with normal cells that do
trigger these these reentry arrhythmias but also triggered by another
made when I italia basic inflammation of the alterations especially of
chemical mediators that are inside the vessel with these very important
another boss unha 2 to which I will return later and that of the worms one
vasoconstriction if we take this as a reference to the crown
we have during the infection could happen on the sudden death is a
severe constriction of the vase a very important space for which the bass is
quits and you have a disease a syndrome that is called prince and angina
marital the vessel his narrow but not from a plaque just from the spasm is one
of the manifestations begins very early so happens with angina printing manita
of ventricular fibrillation are different mechanisms a disorder there is a
son
feel still like this or better better much better maybe there was a cable
underneath that was disturbing here is the community linked to
other walls due antibody formation however did that the spike to
a sequence homologies with this protein for which they can be formed
antibodies that are going to attack the protein itself
structural of the heart so here are the consequences of these types of attack
I think she silicans fling titin antibodies for the falling pitina
just an extremely important finding
from studies that are also fairly recent even less recent because on myasthenia
gravis just has been looking for these we are looking for I felt bodies
if I can have another photo what it's called is a photo where you believe the
contraction the filaments kitchen minds those thin and those spaces
here is perfect then this photo indicates the proper unity of contracts and
of the myocardial fiber and consists of a part that is called sarkò mero
Levete there are c dell strips and yellow and darker recipes
orange and the orange ones know, however, of another mongiello color
made up of my supper while the thin filaments are made up of the
spine as the contraction of the heart muscle occurs through a whole
series of trials also with calcium release but in the end thing
it happens these filaments of my aptin end flow between them inside them is
I just reduce the ser as I was right in the contraction
through this sliding the sarcophagus is shortened and the
central area which is the one that is present and when the fibers are stretched
dilated we can see another image to another image and immediately after
this is practically seen the titine that is a red filament
then what is this titina it turned out that there is not only my china e
can but there is also this titin that you owe
imagine as a custody just like a child imagined the thread of
straight linen on which hung in some ways the myosin e
so when the tt in my china are normal they don't have any alteration lo
scrolling occurs in an excellent manner therefore both internal aggregation
inside of china and of the actinà when instead he found the photo
what is this filament that is killed red chin where and is an image
colored with a very red confinement when this chitin comes instead
attacked by these antibodies and also myosin is one
you can imagine how a shortening is shorter than heaven which is shorter
then the fact that it is shortened shorter more pulled does not allow the fin
an end to the harnesses of rentals or of musina to and perfectly intersect
it remains a bit so look at my hands since the photo does not help you here
normally they come like this and instead they stay like this it is only so precisely because
there is this shortening then this what it entails from a point of view
pathophysiological for which there is a very particular reaction at the level of
all of his wine schoolchildren but also cardiac that if we are referring precisely
to the heart the two-phase heart the phases are diastole when it relaxes
it is the sisto lai when the fibers get shorter and does so almost fills it will do
from carry and almost and strips if this mechanism is altered what happens
he cannot contract perfectly or unfold properly
perfect we must imagine the fiber of the
elastic heart if I have a rubber band that I keep
and then I leave it not behind with mine nor after
then and then i leave it what happens practically i have one
retraction the stretch even more tightens even more but if this
mechanism is inhibited by these antibodies and by the actions on the onesie io
I have a heart look that does so and so but cannot make a complete of
complete Asturian system this thing definitely entails involves a
impaired functioning of the heart here this is the titin you see a little in
those filaments you see the red filament infinitely red is what goes
wait for my dinner and lets china minds of hp nor news in ad
perfectly Latin intersecting is just a filament that you see I don't know
if you can see it you just see that it holds straight up like the
straight line then myosin can come back to me then what happens in
all this happens is that the heart is not working as it should have
one can compare this has more or less action of a cardiomyopathy
restrictive when there is also a dysfunction of the systole of the
diastole or even more likely to a constrictive pericarditis and what is the
for the guard it is positive and the pericardium which padded filled with tissue
fibrous better wraps this fibrous tissue more and more the heart without giving it
the good possibility of expanding to contract leading to what one has
major heart failure so I think I have more or less got the idea
yes we have in this case more than one heart failure more than one
mechanism that can lead to death then improvise to something more
progressive that maybe even lasts over time and maybe afterwards we pay for it
towards the end of what are the monitoring to be done
here then and the other the other aspect is extremely relevant is the consequence
of the pulmonary complication on the heart not because the problem of the
multi-organ damage and in particular of the municipal one has effects
on the hot activity charged so in this case instead what happens
then in this case I should leave for a moment to hint very well if not
I take too much wind on the heart can see a picture of the heart here look
in this way we have a red part is a blue part is exactly
then speculate on the bass trejo a whole left part of the heart
on the left all the right part of the heart is the heart is made up of four
2 upper rooms which are two smaller rooms which are the atria and 2 in c
liori which are my frigoli if we see the red part from the red part
there are vessels coming from the lung which are the pulmonary veins
they enter the small room which is called between the left and door in the blood
oxygenated from the lung into the left ventricle
if you look left and right then the blue part and the red part you see
that the red part and to the musculature that is that of the left ventricle that
it is a much more important musculature than the blue part which is the
right ventricle then blood exits the left ventricle through the
contra through the pumping action of the heart
which is the most important action of this organ and is entered with force
that's why you become the left one must have good musculature and must
work well come on but they a circus what it does circulated in the other organs
in the periphery and to carry the original tissues oxygen this blood then
it returns it must return again to the heart but as it returns it comes back loaded with
toxic substances but above all carbon dioxide then yields
the oxygen to the tissues and indie eye transports of carbonic drinks as it returns
this blood on the other side of the heart on the side of the heart simply returns
for a negative pressure that is inside the rib cage therefore
consider how this blood is sucked into the cage
thoracic and returns to the master milk and then back to the right ventricle on the
question i was asked exactly what happens when i in covip a
interstitial pneumonia and I have an involvement especially with one
production of emboli that come from the periphery
they enter the right ventricle and go into the lung
they go into the lung and determine what a sudden increase in
pressure inside the right ventricle what did I tell you
the left ventricle at 11 neckline important for turbo to bear a
noticeable increase in pressure without relative suffering but a
right ventricle unless used in bronchopathic packs
chronic for which a pulmonary pressure has already established gradually with the
time if instead it goes towards an obstruction of the basic hormonal for micro
my boy or thrombus right on the pulmonary arteries
the right ventricle suddenly encounters a pressure of one hundred
works with a very low pressure with version 10 15 is a sudden
pressure of 100 does not allow the right ventricle practically to
answer is the ventricle stops suddenly stops with a shock that
it is a typical shock of the right ventricle and look at that it is a shock of the
left ventricle we manage to take it but the shock of the ventricle
right is very difficult a fool so dramatic to be able to take it back yes
he may try with a reflexive series etcetera but it is really a situation
really dramatic very often they are lost so patient for
massive pulmonary embolism then I would like to return to the top instead
involvement of the vessels because we have said that this inflammation
especially mediated by interleukin 6 leads to inflammation of the wall
internal vessel of the vessels of the arteries of the veins of infanticides
determining what the vasculites are now if we transfer this freight
to the heart and coronary arteries we have inflammation of the
coronaries that go to exempt what unfortunately when the endothelium becomes inflamed
we will see it in the final part of our chat involves the trunks
and when they have blood clots that can close the coronaries both
characteristic heart attack or angina of ramos and romania and cruz is completely
determines necrosis of the tissue we will certainly talk about but with a waiting heart attack
card is characterized by what from the pain there is the photo of the put with the heart
now I would like to talk to you just for a moment about pain because I believe in
homework section is extremely important because it happened to me of the
home treatment of patients also treatment of people who are
affected by ok and very often or both a pain in all muscles and then one
Diffuse myalgia also affects the rib cage and is also a pain
pain is consequent to the cough that often not always but often accompanies
this section with stops at times annoying due to difficulty and dryness
continues and therefore this too contributes to creating pain
inside the rib cage then this thing of the define to look for the
referral a pain that may be cardiac from a
pain that may not be is not always easy I warn you but I want to give myself
only minimal indications are clearly invaded by the experience that
I can have on purely cardiac pains
if I have pain that affects the rib cage and is accentuated
noticeably if I do acupressure then at that point
especially in pain embedded in the air and likely that pain is
secondary to this whole situation of my daughter therefore of pain that there is
widespread in the body that is I have a pain that is more referable to the central part
sternum with a feeling of constriction or even sensation
that undermines even more anguish I can give you a piece of advice than if you drink
a glass of water a sip and if this is due why can simulate a
killer esophageal heart pain therefore that is causing this pain
6 of its kind space I just take that sip of water from
glass immediately the water passes into the esophagus resolves the spasm and the
pain passes immediately this is another mark of distinction
but there is another are other signs that must make you pay attention and also create
a little bit of a warning about chest pain and if the pain goes with one
cold sweat the cold sweat that accompanies heart pain
always a sign to be very careful and if this shaped retrosternal pain
of constriction or of weight but certainly the maximum and then it is radiating towards
the down is even more so from judo towards the jaw
if you don't have dental problems those contemporary radiation chest pain
constricting in the editorial office at the united bola makes you shoot towards a heart pain
to a percentage actually more than 80 85 percent
and so even if the pain is glad in the arms
both arms to the left arm we say that not always that easy
because you consider that in the category of heart patients
I put you to those who diabetic to diabetic really have a pain threshold
different they have only one the pain enough high excuse me so they perceive
a pain in an at least violent way compared to a subject clearly that
I would not say that then I gave you some
limitations that I can be free minutes or given precisely is placed because the
heart in the sick co lead with chest pain there is a really crap time
of panic and confusion therefore at least some general indications
I would like to talk to you where instead of a particular heart disease which is one
stress heart disease and that is called tako tsubo because I want to tell you about
this is because this heart disease generally has a Monday percentage
strikes in the percentage of the morning of 17 percent instead today they are
finding an increase of 8 percent in erakovic
but this should not surprise us because we are living in a particular situation
stress and this is a heart disease due to the stress you may have
the image I eat them and there are three hearts and a flask that's exactly
then look to the left by now we have learned to know the heart
you see it is well left danger orange and tipped and have all a bit to a
narrow apex now look right to right what comes out instead
an image just like that flask is tako tsubo now I tell you
because it is called that and from a rounded tip proper comes and from
octopus and basket csupo in fact the first discoverers of this syndrome ai
it was Japanese doctors who immediately compared this image
of them as they saw it they saw it with the echocardiogram at the port basket
with which they were welcomed because it is due to a stress because it is due precisely to
moment of the na ships and retina narrator that i told you i am i
Sympathetic nervous system mediators involve a stressful condition
our body an increase in these mediators and this can occur
pathology because it is important because it has pain that is exactly the same as
pain of wrapping the markers that with increase of the markers
it is of damage of the heart and therefore troponin increase and therefore it works
exactly with a heart attack when you make her coquard of branches and you are patient you have
the suspicion with this image of a tako tsubo is what will be the confirmation that
that it is tako tsubo because when the coronaries of the choirs are done
they are free, absolutely nothing is found and then why this disease
the distance of six weeks is diminishing, that is, checks should be made and
then we go back to this ok we can go on then and the other
interest or particular of which I have spoken a lot is what is due
to the va darkened and that is to the formation activation above all comes elements
schoolchildren courts that are found in the blood that platelets gentlemen and may have but
the image one where not the other where there is collagen
here is this then what happens the endothelium is not a structure in itself
given this taylor which is the wall that covers the vases, it is not a structure in itself
since it is a structure that contains I told you these chemical mediators
chemical mediators have a different action they can be escaped big to so many
vasoconstrictors then the low economic mediator of the many more
important that we have level of the cut world and the microse oxide is
really it is his action at the editorial level is very important because
determines a vasodilation and does not already work even the application for
disqualifies and so does prostaglandin 2
instead what is the mediator that is lowest builder mannella and ours
cell 2 is that just cial is arrived
gestine and has its own vasoconstriction effect because nothing comes into the
our body if not with very specific reasons
if we see from the left side of this image we can see that it is there
a celestine spheroidal form is that the platelet this castrine to a charge
negative and this negative charge causes the platelet into one the power
normal as that which on the left does not read the endothelium does not adhere to it
shinde pavia slips into the blood and if we look at the right side what it is
success there is an injury who gives the injury
we said that the interleukin leads by the same virus of this states
for the thorium flame that determine our body ok so it is an endothelium
that presents injuries the first action that is done the purpose
because as if it were a wound it is what it is in all the pinks that I am
possible from the collagen that were previously inside the preta
of the endothelium come out and what they do causes platelets bound by a
holding factor that is released just fine in the hotel or the factor
gifts of in den brandt and tissue factor that is minimally found
also in circulation in the blood but above all there is lan and endothelium
allows the platelet which is normally I told you for charge
negative does not adhere to the endothelium to make its first action what is its own
first action the adhesion to the endothelium through the
factor convinced that she platelet race to the endothelium we can go
next after adhesion the plate what does it do
the other image after joining the plate what does that first thing does
joins there is another image operates where you see the large plate
perfect drive then you will see left to left we have a person with i
large which coiffed to come to the endothelium begins activation
of platelets and so what happens platelets have a change you will see
that form many many spikes these are called slopes or do pd
and then it comes from granulated to large and forms these lace after
let's also go then you did after what let you allow you to have
you see that now they are all aggregating it is an aggregation so yes
it forms a stopper which then tightens the adhesion of the negation
platelet aggregation you see in the yellow table below we have two
points of aggregation due to the so-called geno that links two sites of agam e
in platelets it is that they are two gp2 receptors of three has therefore from this then part
the coagulation cascade and from there the thrombus that the caring is formed
ok if then explain the difference between antiplatelet anticoagulants no why
however a substance that is widely used for the treatment of
kovida just the heparin however when we are in an anticoagulant situation e
antiplatelet we have already seen that platelets and have a different phase
adhesion is aggregation then there are drugs that act precisely
as antiplatelet agents therefore in this first phase of the plate, that is
platelet gets stuck in its aggregation and that's one thing
extremely important because it does not give rise to everything that happens next
acetylsalicylic acid with that aspirin and nikki beach is that
famous thromboxane dvd I spoke that is, it goes to act by inhibiting the very
set that is in charge of the thousand favorite aggregation compulsion houses
how it works there is nothing from cdc I say causing a block of the cycle
oxygenase is then part of the production of arachidonic acid which
eni from ties that is c from c I judge the reported figure is a
irreversible bond while other NSAIDs also act on the thrombus stano danny
time are on cyclooxygenase but with reversible bond therefore the difference
between la spina and other singers and grianti is this then there are other friends
aggregating you remember a single yellow bank with two gp2 b3 sa receptors
very well there are antiplatelet agents that act precisely by inhibiting that bridge
fibrinogen which causes platelets to join and platelets to aggregate
this with regard to platelet aggregation than the former
then we leave instead as the doctor asked me instead
anticoagulant which and anti-coagulant par excellence by the praying team for
excellence in this case heparin acts as the panina le carina acts
on an extremely important substrate that el antithrombin 3 and what it does
paline the heparin causes the anti thrombin 3 mag i the thrombin and therefore
once they are both bound then the heparin binds the anti rubin
to thrombin the thrombin can no longer be used and therefore processed
fibrinogen in fibrin yes I sell this chain clearly me
i cannot have fibrin formation and therefore i have a cascade
coagulant because it never came to the formation of fibrin because I have the
thrombin which is bound and does not allow transformation is the activation of pib
rhinogen in fiber now because heparin is important because normally
in our body and others thrombin and what function a is exactly this
it works badly for them na what you do risky thrombin amplifies the action
that is, thrombin causes thrombin to act 30 times more of its own
30 times more than what it normally does in our body then
strengthens we can of relationship and drags her from here comes a decision
extremely important sometimes heparin seems not to work but does not
it works when the ancient ondine is missing because if that substrate is missing, the heparin
noah does not know how to act so this is the anti-coagulant action
and of the extremely important heparin in fact in phase two the sentence
pulmonary we have two main drugs in the
treatment which are anti-inflammatory cortisone and heparin
anticoagulant because simultaneously with the famous inter-light 6
mice are formed and therefore are one of the widespread thromboses that pop are
then go also enrolled the organs but as assured we have two other drugs
which are the normal anticoagulants called cities or which falls within the
coagulation cascade the band the protein k which falls under all the factors of
coagulation and now which instead are the new oral anticoagulants that act
so the lowest loot on factor 10 by activating blocking the cascade
factor 10 factor 10 then activated too
nixon are part of the yes population year I believe this part
in short, we finished it very clearly very interesting then and
as for last because we have two other important arguments though
we are now delving a little into what kawasaki syndrome is and that
let's say it manifests itself mainly in children mechanism the impact always on
on his kawasaki heart that you don't know what I feel has centered on this question
because I had put the disease and kawasaki pro made in the senate for what
what it does what we have seen during the coronavirus we have seen that from disease
of kawasaki and had a really higher incidence than normal
the incidence of the disease because in the meantime we see what we are
nor does it challenge this disease and kawasaki has been studied in japan in 1967 since
a pediatrician called just kawasaki and the etiopathogenesis has not yet been
certainly maintained it has an actual genesis
the one logical and probably genetic because some people are just that
they develop kawasaki disease is generally are populations of the world
Asian, however, they are also seen here in
coinciding precisely with with macron to viruses
we have kawasaki disease one
inflammatory involvement of small and medium caliber vessels
therefore we have a first phase of the disease which is always here with vasculitis
it behaves with we think therefore in the first weeks the high fever
we can see some photos is the characteristic language is the language
characteristic is described as its own strawberry-colored tongue takes
this coloring the other photo and then they are also skin rashes and they are
always due to these things always raises darkened therefore injuries of things and you
will have an increase in platelets on examination you may have
inflammations of the conjunctiva of the conjunctivitis and of the pupils and hands
and the feet this is all the first phase of
disease lasting one, two, three weeks, therefore more or less with these signs
characteristic you can make a diagnosis of kawasaki disease is one thing from
also important to point out that from the fourth week
the disease you can have either not always luckily it is a percentage that
it ranges from about 2 percent of coronary involvement what what
both for coronary infections this is coronary do not always go in
a 5 percent dilate is only one percent
meets a coronary music with aneurysms I can show in
Other pictures
the last one of the heart looks like a pencil
here is perfect to us in these magical as you can see and there are vases
which are thin straights and then there are like circles and what are those
then look for sure are the aneurysms in fact when I visited and see
i did echocardiograms to children with kawasaki disease they asked me
always going to see the coronary arteries, but not always easy to see
precisely because the kawasaki also involves an involvement of the coronaries
okay ok and then these too will be checked in the post covi dei therefore
ryabko concludes with the post korg monitoring speech because obviously
beyond the possible acute or short-term effects that there may be the
long cofide therefore for heart complications really become
significant and require monitoring over time here's to go to
evaluate the heart muscle compromise so if you want to talk to us a
little and of this unprecedented nose to what he did and what they are
possibly the possible markers to keep under control
I could leave and eventually get out of the kawasaki that is, since I said yes
it can also have an involvement of the coronary arteries
is this disease must be followed and therefore what checks should be done
child who has a kawasaki after the treatment etc. that is a
treatment do you know in front of immunoglobulins etc. we have to do
blood count check because he sure said it's a moment
of platelets we must check all
inflammatory indices because in the fifth eighth week the disease is waning
and the demonstration that this scene disease noticed precisely at the reduction of
all the indexes of inflammation that we are going to do then we must do for
what I told you a two four and eight echocardiography check
weeks and if you go to find a dilation
coronary artery also checks must be made there and if so
form those balls that are the aneurysms must also be evaluated
agonisms that can be as small as 3 mm and more easily
resolvable with therapy always because in this case asa antiplatelet agents are used
platelets because they can complicate thrombosis
inside is even larger aneurysms which are larger than 6 mm
in that case the treatment will be done just as well as arlina a
spa level during so this is one of the important monitoring that you have to
in addition, coronary arteries may be subject to plaques and therefore
develop even at a young age kian kawasaki a kawasaki disease
thrombosis and heart attacks so when you go for other investigations you can
to do too is a survey like stress test to see if it also arises
pain and then at that point then you have to go to study
or you can study coronary systems that are much more advanced than
advanced research which are the acg 64 multilayer tacs i believe is layers that
it gives the possibility not only to highlight the plaque to highlight one
extremely important thing of the Polish
if that plaque is a plaque with a good fibrous cap so don't
it will never break or if a plaque rich in fat and with tissue instead crumbles
very scarce fibrous which could break and that gives for sure
of the indication of more in-depth studies then the disease of
dallas to those who have a really important ditch
then I talked about myocardial pericarditis myocardial pericarditis definitely
must be checked and subsequently with all the indices of
inflammation is the antibodies can also be searched for what I told you
own of the titina but you can also do some checks as well as I know of
checks come with the logistical hole of black, which also has significance
of persistence of a challenge friezes situation also goes to check with
echocardiogram who developed I eat cardio pericarditis for what you get there
I mentioned earlier because it is possible to have constructive pericarditis
what do these positive pericarditis do when I go to study patients with
for the capita constrictive alas sometimes they have an evolution even enough
rapid but it is not always evident that they have developed pericarditis
constructive meanwhile we see the thickened pericardium because this
pericardium a rich in fibrous tissue is the famous mechanism for which the
blood is sucked from the hogwash towards the right ventricle and does not happen
it happens with difficulty and what happens some of the blood fails some
quickly in the right ventricle and where it accumulates it accumulates in an organ that
the first organ of passage to arrive then to the heart that the liver
why these patients begin to develop dilated vessels is one
situation of decompensation which is a right decompensation from a left and therefore
you will also have swollen legs etc. but dependent on the fight
this is at the level of the liver you will have a fluid overload at the level of the
cold that can lead to alteration of the biliary tract of the dl
of the hepatic pathways also causing quite serious pictures that can
evolve then also in cirrhosis or said it is in me because the intervention still takes place
then proposes the extreme cases proper extreme because still burdened with one
mortality high enough that the pericardium tomey to ie cut the
thickened pericardium still carries a mortality rate of 40 percent
so you really get there when when you can't do without it e
so these are surely some paintings that I have described to you that go
checked the controlled also the attack on hbo because its
practically at 6 to 6 weeks and should no longer have with the ad framework
echocardiogram more or less this than what we have said up to this point
time of post col in a couple of questions we can people in therapy
coumadin against co lead effects on blood vessels and heart and I have not
understood the first cause of the demand made in itself are protected against the effects
I say of the copit on the heart blood vessels we say that consequently for everything
what we said who does treatment with own anti-coagulant
for everything I've said so far it definitely has one
in fact, it protects the patients who are at the best
they develop copit is that they do treatment with coumadin the first thing to do and
don't stop your morning treatment for two reasons one because you have it
they meet at the gothic theater and then a disease that develops thrombosis
I already do a drug of that type I am not going to suspend two because if
I do a treatment with coumadin and I am doing it to protect one
mechanical valve are cnr 253 is also a even a little more I don't go
absolutely to suspend it because I'm going to dominate the valve ditto if I
I do a treatment with open coumadin boxed our deep or still
more for a valvular atrial fibrillation yes so my answer is yes
it is clear that you are protected but I always answer that every person is a person a
on its own what it means that if the immune system undermines
answer in a way i will answer in way 6 the immune system nino
answers in another way I will answer another way so if I do the
treatment of which each I am sure protected but if I the
abnormal macrophage response an excessive increase in interventions in the
you are aiming to determine into the knee you could also develop less
easily some others for boxwoods but in general I am protected
then I do not know if this more for the life of the vaccine there are anticoagulants here
let's talk about the presence of of tirana
this app is more related to the presence of some types of antibodies than
they bind to the flour the cardiac aspect I would say that we must talk about the
thrombus formation maybe we will talk about it with another doctor
that we will call in a couple of weeks I think so yes they are published
ham there could be refuses sale from the country perhaps in the cassino road
antonietta asks if it is important to take omega 3 and omega 3 it is
assumption it is a beautiful hot but from this is that it is not just of
heart protection because we know that omega 3s are those fatty acids
and that are good for our body, therefore I re-enter the atherosclerotic plaque
in the speech practically of the protection and development and the plaque
etcetera hand mediatre mind that it also falls on the intestine because
when the virus infects it infects and when I have the right balance of omega 3 e
or a gut that doesn't go towards chronic inflammation and disease
hyper inflammatory, that is, I have a moment not of the
omega 3 and therefore it is not the right balance in our diet and a little man
omega6 and or that motor situations yes yes useful
ok then there was another question that whoever is being treated with ics jana is more
protected towards the covip yes yes for what he said yes also
this is because they always fall within the cumulative axis
and therefore has a form of protection definitely the latter which consequences
precautions for those suffering from supraventricular tachycardia then i
given gazzi and supraventricular we say that the patients developing rhythms and I
I focused on the most important arrhythmias which we are in
and most important ne ventricular rhythms for the technique strongly of pouring that
evolves with ventricular fibrillation instead it has been seen that it is a high one
percentage of Italians who have supraventricular arrhythmias and also
I can already be directly valid on my own I have arrhythmias
supraventricular one of the areas that are written precisely the fibrillation
atrial let's say the covip
it is not that it interferes in a particular way on his person that he has
of supraventricular rhythms but since we have seen why
determines arrhythmia due to alterations within the muscle structure
could this person have an increase in those arrhythmias and devolve
then also the pepe trial report and no severe ventricular which is another thing
well then i really like doctor adriana privitera thanks to
doctor the half ball legs that we will meet in the next appointments e
we hope so but it was certainly an evening full of information
ancient obviously the episode remains available for those who want sum
look at it when thank you and goodnight everyone thank you thank you