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The Cardiac pathophysiology of Covid-19
The Cardiac pathophysiology of Covid-19

“Findings emphasize that Covid-19’s myocardial pathology predominantly arises from fibrin thrombi within the coronary MICROVASCULAR network, especially in the abluminal spaces.

➡️This pathological process leads to myocardial fibre injury, necrosis, and ischemic changes( = fibrosis), contributing to both the acute symptoms and long-term sequelae (Long Covid).”

·x.com·
The Cardiac pathophysiology of Covid-19
SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection
SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection

Using stem-cell-derived vascular cells, researchers found SARS-CoV-2 infects smooth muscle cells (SMCs), not endothelial cells.

Infected SMCs cause inflammation and clotting factors, explaining vascular issues seen in severe COVID-19 cases.

·biorxiv.org·
SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection
COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type | Arteriosclerosis, Thrombosis, and Vascular Biology
COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type | Arteriosclerosis, Thrombosis, and Vascular Biology
“COVID-19 at all levels of severity was associated with significantly higher risk of MI, stroke, or all-cause mortality over 1003 days of follow-up."
·ahajournals.org·
COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type | Arteriosclerosis, Thrombosis, and Vascular Biology
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
“Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis”
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
·medrxiv.org·
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
The acute phase of was and is misunderstood by the majority of doctors.
The acute phase of was and is misunderstood by the majority of doctors.

“Medical images show us that the severe lung disease of #COVID-19 is the opposite of influenza - it occupies a different anatomical compartment in the lungs. All of this means there is no reason to expect that the later phases of COVID-19 should be anything like influenza.”

·x.com·
The acute phase of was and is misunderstood by the majority of doctors.
Table 3 Adjusted hazard ratios (95% CI) comparing the incidence of arterial thrombotic events after versus before or without a COVID-19 diagnosis, in the pre-vaccination, vaccinated and unvaccinated cohorts, overall and according to COVID-19 severity
Table 3 Adjusted hazard ratios (95% CI) comparing the incidence of arterial thrombotic events after versus before or without a COVID-19 diagnosis, in the pre-vaccination, vaccinated and unvaccinated cohorts, overall and according to COVID-19 severity
“Adjusted hazard ratios (95% CI) comparing the incidence of arterial thrombotic events after versus before or without a COVID-19 diagnosis, in the pre-vaccination, vaccinated and unvaccinated cohorts, overall and according to COVID-19 severity”
Adjusted hazard ratios (95% CI) comparing the incidence of arterial thrombotic events after versus before or without a COVID-19 diagnosis, in the pre-vaccination, vaccinated and unvaccinated cohorts, overall and according to COVID-19 severity
·nature.com·
Table 3 Adjusted hazard ratios (95% CI) comparing the incidence of arterial thrombotic events after versus before or without a COVID-19 diagnosis, in the pre-vaccination, vaccinated and unvaccinated cohorts, overall and according to COVID-19 severity
SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels
SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels

Autopsy study in patients with COVID shows that: SARS-CoV-2 infects, replicates and persists in Macrophages within the coronary vasculature Since CARDIAC MACROPHAGES have a half-life of 8.8years they would act as VIRAL RESERVOIRS in Atherosclerotic plaques

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels
·nature.com·
SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels
The Main protease (Mpro) from SARS-CoV-2 triggers plasma clotting in vitro by activating coagulation factors VII and FXII
The Main protease (Mpro) from SARS-CoV-2 triggers plasma clotting in vitro by activating coagulation factors VII and FXII
“Although the connection between COVID-19 and coagulopathy has been clear since the early days of SARS-CoV-2 pandemic, the underlying molecular mechanisms remain unclear. Available data support that the burst of cytokines and bradykinin, observed in some COVID-19 patients, sustains systemic inflammation and the hypercoagulant state, thus increasing thrombotic risk. Here we show that the SARS-CoV-2 main protease (Mpro) can play a direct role in the activation of the coagulation cascade.”
Although the connection between COVID-19 and coagulopathy has been clear since the early days of SARS-CoV-2 pandemic, the underlying molecular mechanisms remain unclear. Available data support that the burst of cytokines and bradykinin, observed in some COVID-19 patients, sustains systemic inflammation and the hypercoagulant state, thus increasing thrombotic risk. Here we show that the SARS-CoV-2 main protease (Mpro) can play a direct role in the activation of the coagulation cascade.
·biorxiv.org·
The Main protease (Mpro) from SARS-CoV-2 triggers plasma clotting in vitro by activating coagulation factors VII and FXII
Harriet Carroll: Recognise vax-induced long COVID on Twitter
Harriet Carroll: Recognise vax-induced long COVID on Twitter

Latest paper from Dr Robin Kerr & me: #LongCovid is primarily a Spike protein Induced Thrombotic Vasculitis https://researchsquare.com/article/rs-2939263/v1 Here we proposed that long covid is primarily a spike protein-induced thrombotic vasculitis, & we use Robin as a supporting case study 🧵 #TeamClots

·twitter.com·
Harriet Carroll: Recognise vax-induced long COVID on Twitter
Jbm
Jbm
SARS‐CoV‐2 spike protein induces endothelial dysfunction in 3D engineered vascular networks: effects specific to SARS-CoV-2, vascular dysfunction caused by an increase in inflammatory cytokines, dexamethasone prevents spike protein-induced ED.
·onlinelibrary.wiley.com·
Jbm
A Case of Deep Vein Thrombosis After Recovery From COVID-19 and Its Association With Elevated D-dimers
A Case of Deep Vein Thrombosis After Recovery From COVID-19 and Its Association With Elevated D-dimers
"Elevated D-dimer levels are a predictor of hypercoagulation complications in COVID-19. Patients with persistently elevated D-dimer levels after recovery from COVID-19 should be screened for thromboembolic complications, even if they are asymptomatic."
·cureus.com·
A Case of Deep Vein Thrombosis After Recovery From COVID-19 and Its Association With Elevated D-dimers
COVID-19 as a Vascular Disease: Lesson Learned from Imaging and Blood Biomarkers - PubMed
COVID-19 as a Vascular Disease: Lesson Learned from Imaging and Blood Biomarkers - PubMed

From 2020: "COVID-19 can be considered a vascular disease with regards to serious complications and causes of mortality...blood clots have emerged as the common factor unifying many of the symptoms initially attributed without an explanation to COVID-19."

·pubmed.ncbi.nlm.nih.gov·
COVID-19 as a Vascular Disease: Lesson Learned from Imaging and Blood Biomarkers - PubMed
Even mild Covid raises the chance of heart attack and stroke. What to know about the risks ahead
Even mild Covid raises the chance of heart attack and stroke. What to know about the risks ahead
The big concern raised by this fresh study is that medium- to long-term harms on the body’s blood vessel network (the vascular system) may be much more common than that. And it could drive a new pandemic of cardiovascular disease over the coming years."
·iol.co.za·
Even mild Covid raises the chance of heart attack and stroke. What to know about the risks ahead
SARS Covid-19 as an immunothrombotic disease and the potential benefits of a new estrogen-free contraceptive containing drospirenone.
SARS Covid-19 as an immunothrombotic disease and the potential benefits of a new estrogen-free contraceptive containing drospirenone.
"As Covid-19 is considered an immunothrombotic disease, the potential benefits of estrogen-free contraceptives like drospirenone are discussed. Adding estrogens in contraception may rise the cardiovascular risk in Covid-19 and Long Covid patients."
·authorea.com·
SARS Covid-19 as an immunothrombotic disease and the potential benefits of a new estrogen-free contraceptive containing drospirenone.
Proteomics of fibrin amyloid microclots in long COVID/post-acute sequelae of COVID-19 (PASC) shows many entrapped pro-inflammatory molecules that may also contribute to a failed fibrinolytic system - Cardiovascular Diabetology
Proteomics of fibrin amyloid microclots in long COVID/post-acute sequelae of COVID-19 (PASC) shows many entrapped pro-inflammatory molecules that may also contribute to a failed fibrinolytic system - Cardiovascular Diabetology
More evidence that LongCOVID symptoms are due to widespread endothelial damage and a failed fibrinolytic system. We again found numerous entrapped inflammatory molecules; and this time also antibodies in microclots
·cardiab.biomedcentral.com·
Proteomics of fibrin amyloid microclots in long COVID/post-acute sequelae of COVID-19 (PASC) shows many entrapped pro-inflammatory molecules that may also contribute to a failed fibrinolytic system - Cardiovascular Diabetology
SARS-CoV-2 Mediated Endothelial Dysfunction: The Potential Role of Chronic Oxidative Stress
SARS-CoV-2 Mediated Endothelial Dysfunction: The Potential Role of Chronic Oxidative Stress
"Endothelial cells have emerged as key players in SARS-CoV-2 infection and COVID-19 inflammatory pathologies. Dysfunctional endothelial cells can promote chronic inflammation and disease processes like thrombosis, atherosclerosis, and lung injury."
·frontiersin.org·
SARS-CoV-2 Mediated Endothelial Dysfunction: The Potential Role of Chronic Oxidative Stress