Many thanks to Prof. Dr. Frank Ruschitzka, who leads the Cardiology department at the University Hospital in Zürich, Dr. Nilam Mangalmurti, pulmonary intensivist at the Hospital of the University of Pennsylvania , Dr. Richard Becker, cardiologist at the University of Cincinnati College of Medicine and to Dr. Peter Carmeliet vascular biologist at the Belgian research institute VIB, for revealing us the endothelial attack, as principal CoV2 mechanism to induce generalized venous micro-thromboembolism that ends in pulmonary and distance organ failures :

https://www.sciencemag.org/news/2020/06/blood-vessel-attack-could-trigger-coronavirus-fatal-second-phase

« This mechanism could explain why the disease pummels some patients who have obesity, diabetes, and cardiovascular conditions: The cells lining their blood vessels are already compromised. If so, drugs used to treat these conditions might help prevent other COVID-19 patients from sliding into serious disease »

Following the up-mentioned collegues findings, we are pleased to suggest, in all modesty, our teams' posible contribution to an endothelial protection (NOs) :

Article All-trans retinoic acid stimulates gene expression of the ca...

Conference Paper Natriuretic peptide and other cardio-protective genes are st...

All that strenghtening even more our first question : Should COVID-CoV2, be called Severe Acute Circulatory Syndrom (SACS) rather than SARS ?

Best, DCM

I don't think so. It's premier and focal attacks and troubles are in and through the respiratory tract and/or system. Circulatory, inflammatory, coagulatory, and immunomodulatory effects may be called secondary or contemporary.

Regarding my knowledge it shows that after SARS, Severe acute circulating problems arises. We can easily say that SACS is a one of the complications of Covid-19. As the pecentage of SARS is higher that's why it is known to everyone.

A very good point. In our stroke center here in Ain Shams University in Egypt we encountered cases who presented by different forms of ischemic strokes in association with positive PCR for COVID ..

Some strokes were bilateral and of large vessel occlusions with cases who were young with no vascular risk factors ..

Even some were asymptomatic for respiratory manifestations but positive for these cardiovascular manifestations and strokes.

And thats why your point is so important i.e. strokes were the primary manifestations in some cases of covid.

Dear colleagues many thanks for your precious feed-backs,

To us, the CoV2 attack looks like a vicious loop : airborn transmision (very efficient, like measles), entrance attack on the respiratory system (once again like measles), vicinity attack on pulmonary blood vessels endothelium, systemic attack on body endothelias, subtle micro-haemoragia, responsive-clotings, thromboembolism, vascular origin hypoxemic disorder, and lack of oxygen in the blood that closes the loop back in pulmonary colaps , with death by suffocation due to a generalized venous micro-thromboembolism. Chess and matt ! Nine out of ten intubated/ventilated people die, according to Dr. Sandro Giannini (ITALY !), because the therapeutic intervention is pulmonary while the causal problem is cardiovascular. Indeed, there is no point in ventilating a lung if blood is not reaching that lung properly. In parrallel, the thromboembolism must also be adressed by any mean : prevented (idealy), dissolved, even compensated if too advanced (e.g. transfusion )! All together tropisms, while clearly infecting lung cells, this virus ultimate target seem to be endothelia cells all over the body.

So, should a new infectious disease reflect : 1) The acces tissues or 2) tissues that seem to be destination preferential target tissues ? Whatever the name, in order to succesfully direct curative interventions, we believe the name of a new infectious disease should reflet the cause of its worse outcomes too. Thanks,

Your contribution, is most appreciated, DCM

I agreed with Dr. Md Rabiul Alam ,

Because Circulatory & Respiratory syndrome are different although the cause of death is due to Cardio-Respiratory failure ie whenever SARS is observed indirectly SACS may be also observed or vice versa .

Thanks, Dr. Datta,

So, given their close causal inter-relation, SARS with SACS, observed in CoV2 attack and further COVID development, we could consider SARCS ( Severe Acute Respiratory & Circulatory Syndrome ) or even SHARCS ( Severe Hematologic Acute Respiratory & Circulatory Syndrome ). Hematologic too, given that micro-clotings, ( with silent but progressive drop in O2 saturation), seem to preceed all further major failures ( either Circulatory and/or Respiratory). An wider evocative acronyme, could instantly recall causes & issues, for better curative intervention.

Best, DCM

I don't believe I am a very knowledgeable person to answer this, but to my precise, during research I was trying to accumulate case reports and data from various centres and hospitals. Those data revealed about the many patients who were covid affected and were reported to be dead due to cardiac arrest.

So, indeed it is so Tamer Roushdy

well Tathagata Dey , in our hospital and its stroke center, an example to this cardiovascular manifestations of COVID was a young male patient with no medical past history, who presented with middle cerebral artery stroke with aphasia following four days of mild chest manifestations in the form of cough and fever of 38.5C, he was stable for nearly 3 days when he suddenly suffered acute chest pain and ECHO revealed recent acute apical thrombus with myocardial infarction, fortunately he was in the hospital and was saved.

and this is just a single example that this virus has many effects on the body and a large proportion is related to circulation. and that is why in Egypt one of the line of management is to initiate anti-coagulation for COVID cases.

Maybe

How COVID-19 affects your cardiac health

Tamer Roushdy Indeed this is a wise step to treat the patients. I believe every country should adapt this, but on a smaller scale at first. I believe some statistical reports should also be presented regarding this approach.

Well, I had a distant colleague's relative who was victim of covid. He suffered fever at first but for 2 days only and it was mild. Then he was completely fit. But the fever returned again after 3 more days and this time it was over 100F and after 1 day he wasn't feeling very well and was hospitalized. The next morning, he went through cardiac arrest.

Would You like to join the conversation? Shreyans Chatterjee .

At this point I suppose we all agree that nine dead out of ten intubated/ventilated people, according to Dr. Sandro Giannini- Italy, does not qualify intubation as THE successfull curative anti COVID intervention ! That is because ventilation is pulmonary only, while the causal problem is cardiovascular. So is the lethal prognostic. I still can not see a point in ventilating a lung if blood is not reaching that lung properly ! So whatever the name will be reframed, SARS , SACS, SARCS ( Severe Acute Respiratory & Circulatory Syndrome ) or even SHARCS ( Severe Hematologic Acute Respiratory & Circulatory Syndrome ), the job of the day is reversing ( or even preventing ) these silent micro-clotings and, the subsequent progressive O2 drop, preceeding all further major failures ( either Circulatory and/or Respiratory). I guess the Egyptiens are on the right track here ( see Dr. Tamer Roushdy up here) initiating anti-coagulation therapy to adress thromboembolism and so to give patients a real chance to really benefit from oxygen back-up therapy. In conclusion I agree with Dr. Roushdy and Dr. Tathagata Dey up here : I believe every country should adapt this, while waiting for the Second Wave ! Best, AS

Dear Dr. Manolescu: In my opinion, SARS Cov 2 virus infection triggers a metabolic shift in the host cells in order to activate glycolysis, thus creating a hypoxic state leading to inflammatory changes in the lungs. The reason for this hypoxemia could be related to the fact that many viruses replicate more easily in low oxygen environments.

Please read this article I just uploaded.

Deleted research item The research item mentioned here has been deleted

Best regards,

Alberto

Thanks Dr. Rubio-Casillas,

I'm afraid you are right as for CoV2 virus inducing hypoxia in very efficient and pluralistic manners , most likely in order to shift the host metabolism to favorise the viral replication. Primitiv organisms seem to be naturally very good in adaptative entropy optimisation, somehow looking as linear algorithms ( Danzig G. 1947 ).Your proposed mechanism seem to be one of them, most likely. Yet Dr. Tamer Roushdy's , and many others, reports for thromboembolism, strokes and apical thrombus, are clinic realityes clearly inducing hypoxia too ! The virus attack beeing metabolically multivariable, so must be our response package. It's good news Dexamethasone impairs production of HIF-1 while diminishing excessive inflammatory response ! But if the silent micro-clotings are already in the system , using anti-coagulation therapy to adress thromboembolism becomes a must. That gives patients a real chance to really benefit from oxygen back-up therapy ! If not, just like Dr. Sandro Giannini- Italy said : « There is no point in ventilating a lung if blood is not reaching that lung properly ! » . So I suppose the best results will come with optimised protocols, adressing both inflamation and thromboembolism, thus hypoxia on both axis, increasing the oxygen-therapy benefits and so leading to recovery. Thank you very much for your most precious complementary contribution. Best regards, Daniel Constantin Manolescu

It should not be called SACS because

1) the cases where patients are showing respiratory/pulmonary problems is more than patients showing circulatory disorders.

2) The lack of oxygen in blood is mainly due to the malfunction of lungs.

So I think this is a short answer to the question.

To call it circulatory syndrome, we are not seeing any actual circulatory compromise say hypotension,hypovolemia. so, its not wise to call SACS.

I personally believe that the involvement of the disease is not only of the respiratory and vascular system, but multisystemic ... including the eyes:

Article The Ocular Surface and the Coronavirus Disease 2019: Does a ...

Thanks Dr. Pateel and Chatterjee,

I guess your contributions are joining Dr. Sima conclusion up here : « whatever the name, SARS , SACS, SARCS ( Severe Acute Respiratory & Circulatory Syndrome ) or even SHARCS ( Severe Hematologic Acute Respiratory & Circulatory Syndrome ), the silent micro-clotings must be resolved, for a better survival » ». We all agree the virus attack on metabolism is multivariable. Hypoxia seem to arrise on three interrelated paths : lung malfunction (Dr. Chaterjee), enhanced HIF-1 in cellular attack (Dr. Rubio-Callas ) and endothelial attack (Dr. Tamer Roushdy's , and many others, reports for thromboembolism, strokes and apical thrombus beeing clinic realityes ). Even some beeing asymptomatic for respiratory manifestations but positive for these cardiovascular manifestations and strokes ! Their anti-coagulation therapy , plus ventilation, clearly improved their patients survival, still beeing the safest way to adress thromboembolism ! That gives patients a real chance to really benefit from oxygen back-up therapy ! If not, just like Dr. Sandro Giannini- Italy said : « There is no point in ventilating a lung if blood is not reaching that lung properly ! » . So I suppose best survival will come with optimised protocols adressing several hypoxia inducers, while still delivering oxygen-therapy back-up. Clearly facing a cardiovascular/respiratory harmfull loop (Dr. Jaydip Datta), a higher relevance acronyme would probably be SARCS ( Severe Acute Respiratory & Cardiovascular Syndrome ). Most appreciated, thanks !

Best regards, Daniel C Manolescu

Thanks Dr. Napoli,

Very important your revelation on CoV2 occular transmission ! And once inside, the cardiovascular/respiratory harmfull loop develops.Now, the eyes beeing related within the ORL net, the next question that arrises is : How about the ears ?

With increasing evidence, anticoagulation is routinely used. Microthrombi once occurred, do not have much treatment to offer, but ARDS needs LPV, proning, etc.

Thus, the name change is not justified. However, Keeping a high index of suspicion for non-pulmonary complications cannot be over-emphasized

Thanks Dr. Pranav Ish

You are totally right : with increasing evidence, anticoagulation is, and must be, routinely used in COVID intensive care, given major cardiovascular related problems (e.g. microthrombi). That makes the ventilation back-up more efficient too ! In time, it will probably be reflected in COVID medical condition name anyway. But for now, the idea is to save as many lifes as possible with specific antiinflamatory+ anticoagulation + oxygenation thérapy. Thanks for sharing ! DCM

Article Data analytics for novel coronavirus disease

May be....because the reaction is different from person to person and area to area.

Dear Andrey,

your analysis is very accurate. In my opinion, a neurological factor should be added as a key parameter, in order to better evaluate the patient's perception regarding dyspnea. Plus, it could be useful to carry out some research, aiming to set an accurate PaO2 thershold value.

Good luck with your work,

Dave

Excellent point. Certainly, thrombotic changes represent a peculiarity compared to previous coronavirus infections.

Thanks Dr. Nioi,

Exactly ! Thrombotic issues representing a peculiarity compared to previous coronavirus infections, I assumed it could be of both, clinic help and taxonomic interest, to reflect it within CoV2-Syndrome acronyme. Following our group here contributions, a fair compromise appears to be SARCS ( Severe Acute Respiratory & Cardiovascular Syndrome ). Most appreciated ! Best, DCM

Thanks Dr. Voskoboinick ,

Both for your contribution and your very accurate and documented annalysis. Many thanks to Dr. Elkazzaz M. too, for suggesting a very relevant paper ( one more among so many others ) on the topic. I would like to share it in our group:

Article Cardiovascular manifestations in severe and critical patient...

Thanks all of you for your precious contributions ! Best, DCM

https://www.researchgate.net/publication/343443325_The_Paradigm_Shift_in_the_Indian_Education_System_during_COVID19_Impact_Opportunities_and_Trends

SARCS ( Severe Acute Respiratory & Cardiovascular Syndrome ). Most appreciated .@ Daniel Constantin Manolescu

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Congratulations!

The question is not how to name the disease differently, but the choice of adequate prevention, therapy and rehabilitation tactics for COVID-19.

You are right that thrombus formation and thromboembolism play a key role in the pathogenesis of the development of the terminal state in SARS-CoV-2. But these events develop along with destructive processes in the lung tissue and disruption of gas exchange in the lungs. It is inappropriate to unambiguously determine which of the pathological processes is the most important. Each patient has individual characteristics of the development of pathology associated with age, gender, concomitant diseases. It is advisable in each specific case to take into account all these factors in aggregate.

Thus the wider compromise in identifying the enemy most deadly weapons target: « Respiratory & Cardiovascular » . Thanks !

This is a very interesting debate. As the pathogenesis of COVID-19 involves immunothrombosis. Perhaps the name should incorporate this.

Perhaps SARCIS?

Severe Acute Respiratory and Cardiovascular immunothrombotic syndrome.

Would be grateful for your thoughts.

Thanks Dr. Rajendram,

Article Cardiovascular manifestations in severe and critical patient...

Thrombosis beeing clearly of cardiovascular origin, one may consider they are already covered by the already inclusive SARCS acronyme ( Severe Acute Respiratory & Cardiovascular Syndrome ). But then after, when it comes to details, anything contributing to identify the cardiovascular dimension as one of the CoV2 most deadly weapons within « Respiratory & Cardiovascular », could be helpfull !!!

I would like to thank Dr. Lora Benoit , California, USA, for her contribution concerning the micro cloting arrival in COVID19 ! Here's her hypothesis :

« Covid disables the IFN apparatus during the course of infection. Ace2 on the vascular endothelium allows for viral entry into the cells. Endothelial cells express pattern recognition receptors, as wells, macrophages below, that can trigger innate pro-inflammatory cytokines (IL-1, IL-6, TNF-alpha), which are delivered systemically through the vessels and induce the acute phase response leading to upregulation of fibrinogen, inducing indirectly, a hypercoag state. Cytotoxic damage to vessel wall as a result of endothelial infection triggers the extrinsic pathway of coagulation, through the release of TF. Platelets are activated by TNF-alpha, causing DIC. It seems that we are seeing much more coag issues here in California. Especially in patients that are inflammatory-polarized at time of infection, including T2D and obese patients » .

Best DCM

Dear colleagues,

There is more and more consensus the COVID-19 is a Severe Acute Respiratoty and Cardiovascular Syndrom (SARCS), rather than SARS only ! Thus it appears we must prevent, stop or at least reverse to some extent those CoV2 micro clotings ! Otherways ICU ventilation wouln't give its full potential in tromboembolism affected lung. So what should we do ? What could work ? Let's brainstorm a bit ! How about temporarly chelating some Ca from the blood stream, the moment one receives a positive CoV2 test ? Mild chelation ! Whitout proper circulatory Ca amount, platelets and fibrinogen activation should be delayed, and so will be the disseminated intravascular coagulation, right ? Maybe a reasonable Citric Acid administration would help in that ? In parrallel allowing these patients some more NO in order to protect their endothelium, maybe through NOs enhancers ? How about lowering circulatory homocysteine in the same time ? That could be easily achieved with some B12, B6 and folic acid administration right ? Some Omega 3 PUFA should also help both as anti-inflamatory and anti-coagulant action ? Some lecithin , beeing an emulsifier, should keep the cholesterol in a fluid status right? Why not some low 89 mg Aspirin too, as recomended in preventing CHF? Would these give enough direct and synergic action to delay or even to stop the DIC ? Anyway once in hospital , heparin should be considered on a regular basis I think. Maybe even before, as in very low dosis, at home in pre-hospitalisation prevention ! And clot disolving medication shoud be considered when in ICU, as like for treating a possible CHF or strokes , that offen are occuring by surprise in CoV2 ICU patients ! Just wanted to submit and to share a few thoughts on that topic ! Best DCM

Hi DCM,

We have alot of covid here where I am living in California. Many of the patients that progress to severe disease recover and then are released from hospital only to experience a coag event about a week after they are discharges. The degree of coag is unprecedented. So they are now sending recovered patients home with standard anticoag drugs to prevent this. They are finding that this in conjunction with a macrolide antibiotic and dex works well.

The lung phenotype is largely interstitial disease. There is massive recruitment to the lungs of innate immune cells. This can be blocked with a leukotriene inhibitor in principle. So my Tx cocktail of choice: 89 mg aspirin, dex, leukotriene inhibitor, azithromycin, eliquis. Since I am at risk and working in a high risk situation, I am taking aspirin and leukotriene daily as well as vitamin and essential fatty acid supplements.

I would not consider NO enhancers as these will agonize the activity of the M1 macrophages and promote additional inflammation.

I have asked about the use of metformin, as it readily converts M1 ro M2 macrophage, my understanding is that this is not as successful as the use of anti-inflammatory macrolides and dex

There was an interesting paper in June that showed the presence of megakaryocytes in affected tissues. https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(20)30178-4/fulltext

Extramedullary megakaryocytopoiesis in known to occur in the lungs under normal conditions, but the scope of which this occurs in covid is extreme. this also adds to the coag phenotype .

May I ask what they are using in Montreal to deal with severe covid.

Dear colleagues,

Retinoids seem to reveal important roles to play in fighting COVID19. On multiple axis ! For the cardiovascular interest here, they may also join the anti-clotting arsenal delaying platelets and fibrinogen activation, in CoV2 silent micro-clotting. Furthermore : « Oral retinyl palmitate or retinoic acid corrects mucosal IgA responses toward an intranasal influenza virus vaccine in vitamin a deficient mice. Retinoids inhibit inflammatory TH17 T cell responses, promote regulatory T cell (Treg) responses, and regulate expression of toll-like receptors (TLRs). A combination 13cis RA & all-transRA enhances Neutralizing Antibodies in COVID 19» to cite just a few from our egyptian colleagues ( Elkazzaz et al.2020). Retinoid beeing one of our main expertise field we thought sharing that info, amid our CoV2 common effort : https://clinicaltrials.gov/ct2/show/record/NCT04396067

Best, DCM

Dr. Zach Bush has pointed out the following: PM 2.5 causes viral clumping, leading to higher uptake of cyanide as well as abnormally high concentrations of coronavirus entering the cell. This causes conformation change in red blood cells leading to hypoxia, and therefore micro-clotting. Many New York patients did not even have immune responses (elevated white blood cells, temp. etc.), which suggest the root cause of such symptoms are not merely because of a virus. PM 2.5 is particularly high in Wuhan, Northern Italy, New York, and other areas where COVID-19 cases were severe.

Hi Jorge, this is a great point, in particular, I would like to mention that there is an enormous amount of literature published on the topic of air pollution / inflammation and coagulation, especially with respect to the PM 2.5. I believe based on local findings here in California, that pre-existing inflammation (obesity, T2D etc) at the time of infection lends to a clinical phenotype underscored by coag. I agree as well on the principle of retinoids potentially down-regulating the inflammatory response and coag events and promoting mucosal response through modulation of Th responses to favour IgA production. Actually, I find the ideas itemized by Elkazzaz et al.2020 so germane that I have asked the lead author to collaborate on a review article with me .

Good evening Dr. Benoit and Dr. Lopez

Totally agree with the fact that any pre-existing inflammatory « terrain » (whatever the causes package ) will only worsen the CoV2 attack outcome and the survival prognostic ! Particularly given this CoV virus' thrombotic issues are representing a peculiarity (or at least they are reaching a much higher extent ) compared to previous coronavirus infections, and that is very interesting ! That points out to a several mecanisms package leading to wide micro-thrombosis ! One of them beeing the CoV attack on blood vessels (endothelial cells ) and their defensive answer leading to micro-coagulation ! Viral clumping indeed leads to higher concentrations of coronavirus entering the cells. Not to forget the pulmonary syncytia observed in CoV2 infected lung, raising the questioning as for the CoV2 virus-induced cell fusion potential in other tissues than lungs. Does viral production and distribution of virus-induced erythrocyte binding sites correlates with progress of fusion ? Does hemadsorption occurres with CoV2 ? An if it does so, would it be predominant within the confines of the syncytia ? We know in measles infections, the erythrocytes are scattered sparsely over immature syncytia, while densely packed in the center of mature syncytia ( Rentier B et al 1978). Anyway, hypoxia is the common result, leading to cellular and hystologic disfunction, then to organ failures ! That digs us to mitochondrias, I would say, and of course to pathologic apopthosis ! Clear proof in that sens are the severe fibrosis, longlasting even in the CoV2 survivors lungs ! Retinoids beeing epithelia protectors and contributors in the cell respiratory chain they might be of some help on several metabolic paths in COVID, and I am happy to hear about Dr

Benoit and Dr. Elkazzaz colaboration ! I'll be arround if I can be of some help ! :)

Makes sense I suppose since it affects the lungs and cardiovascular system more severely, although, it also affects other cells that have ACE 2 receptors such as intestinal cells and brain cells.

Perhaps it is named "SARS" because it belongs to the same group as SARS-COV-1.

You are right Dr. Halim an for sure the SARS-CoV-1 served for the SARS-CoV -2 etymology ! Yet, at this point of the COVID pandemia, it became clinicaly proven thrombotic changes represent a CoV2 peculiarity compared to previous coronavirus infections, just as Dr. Nioi, Dr. Roushdy and other colleagues have previously quoted here. So anticoagulants beeing now a must in the COVID therapeutic protocols, either preventively ( 1-st or 2-nd prevention) or ICU, for survival prognostic improval! Cardiovascular dimension beeing CoV2 caracteristic it should be acknowledge as such, to direct and speed therapeutic interventions !

Please check one more slide with the statistical information: after 6 months of pandemic statistics of covid-19 cases have been showing fantastic stability in being largely confined to the 30-50 degree belt (92%-97% of the world's totals).

Thanks Dr. Kondakov,

Very interesting hypothese and associative data in support ! I understand you suggest there might be some exobiology « software» component into this new CoV2 virus, while still harbouring some Earth still « harware » ! So a « chimeric » ! That's hot ! Yet, can you better let us know what does this has to do with the COVID main lethal outcomes : lung tromboemboly via general blood microcloting, specifically associated with this CoV2 virus ? Would that be a « software» part ?

Following the best answer.

Dear colleagues, wishing ...a Better New Year 2021 !

Our research team has just released the numbers of our vitamin D clinical snap shot survey in Montréal :

Preprint Vitamin D homeostasis in obese and diabetic groups, potentia...

In regard to the COVID-19 immunity challenge, the need for a vitamin D supplementation seem to be obvious.

Best, DCM

Hello dear colleagues,

So now, a little bit further down the COVID's road, here's a cardiovascular update:

from THE AMERICAN COLLEGE OF CARDIOLOGY 2021 Release

https://www.acc.org/latest-in-cardiology/articles/2021/04/21/13/08/intermediate-and-long-term-impact-of-covid-19-on-cardiovascular-disease

It speaks by itself I would say! They might have to deal with longterm CV risk too !

The virus should be names as per the viral nomenclature and also based on its place of origin

Thanks Dr Barh,

Totally agree and that is why we've got names like CoV-2, beyond the viral strict scientific taxonomy for the variants, not that much vernacular to people :) As for the « place of origin », the greek alphabet was politicaly-correct employed to avoid ethnographical or geopolitical stigma, as you know :) Back to symptoms now, we must admit that while SARS speaks about entrance (airborn virus) and primarly impact, SACS speaks about the « clotting storms » that turns to be fatal for many.

That's why avonding it when defining a « syndrome » keeps it uncomplete I think.

A coherent compromise would be:SARCS for the CoV-n (by now) wide syndrome.

Thanks for contributing, DCM

Dr Daniel Constantin Manolescu

This study tells you the story of heterogenous presentation of late thrombotic complications in COVID-19 and the relevance of prophylactic measures against the hypercoagulability.

A healthy patient with less severe COVID-19 and sub acute mesenteric venous thrombosis after the onset respiratory symptoms which was characterized by occlusion of abdominal veins leading to intestinal ischemia and necrosis. Hypercoagulability is the state that may result thrombotic complications.

Link is below:

Article Subacute Mesenteric Venous Thrombosis secondary to COVID-19:...

Thanks Dr. Kaushal, Totally agree ! Best, DCM