“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).”
Long Covid patients exhibited persistent endothelial dysfunction.
This was indicated by lower venular flicker-induced dilation (vFID), narrower central retinal artery equivalent (CRAE), and lower arteriolar-venular ratio (AVR).
“Our results demonstrate that prolonged endothelial dysfunction is a hallmark of PCS, and impairments of the microcirculation seem to explain ongoing symptoms in patients.”
Great analysis thread:
“SIGNIFICANT NEW STUDY PUBLISHED TODAY IN NATURE!
Fibrin ‘binds to the SARS-CoV-2 spike protein,’ forming clots that ‘drive systemic thromboinflammation and neuropathology,’ and it happens ‘independently of active infection.’
Simplified breakdown of the paper below!
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
"I hope to god I'm wrong. I've never wanted to be more wrong in my life.... Worst case scenario... we are going to see a tsunami of cardiovascular disease over the next few decades." #LongCOVID
