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A Comparison in Short Term Outcomes of Coronary Artery Bypass Grafting Surgery between Post-COVID and Non-COVID Patients 🚨So AGAIN, Post-COVID patients after bypass surgery suffer nearly DOUBLE the arrhythmias (48% vs 26%) and kidney injury (38% vs 16%), plus days longer on the ventilator and in ICU. Prior COVID is not ‘just a cold’ for cardiac surgery!🫀 ➡️An interesting small comparative observational study(July 2024 to June 2025, 100 patients with CAD were included, half of them had no previous history of COVID-19 infection (group A), other half had history of covid-19 infection (group B)). ➡️Key findings: - Post-COVID patients had significantly higher rates of cardiac arrhythmias (48% vs. 26%, p=0.023) and acute kidney injury (38% vs. 16%, p=0.013). - They also required longer mechanical ventilation (11.8 ± 5.2 vs. 7.1 ± 4.7 hours), ICU stay (6.9 ± 2.2 vs. 4.9 ± 2.4 days), and postoperative hospital stay (10.6 ± 3.3 vs. 8.4 ± 1.8 days) , all p<0.001. - Re-exploration (10% vs. 2%) and mortality (8% vs. 2%) were numerically higher but not statistically significant. ➡️Post-COVID patients undergoing coronary artery bypass grafting(CABG) may be prone to experience worse short-term outcomes and face longer recovery periods! ‼️So, prior COVID-19 leaves a measurable residual burden: even after recovery, these patients face substantially higher rates of serious postoperative complications and markedly prolonged recovery after CABG. The physiological impact is clearly not trivial. ‼️IMPORTANT: Results are consistent with the broader literature on residual COVID-related vulnerability in the perioperative cardiac surgery setting, especially regarding recovery duration and certain organ-specific complications! #AvoidSars2 #AvoidReinfections banglajol.info/index.php/MED…

Epstein–Barr Virus: More than Just an Infection 🚨EBV isn’t “just mono.” It rewires B cells, mimics host proteins (GlialCAM → MS, nuclear antigens → lupus), drives lymphoma and paediatric cytokine storms, This new Belgian review also flags emerging, not yet solid, evidence that EBV reactivation after COVID may contribute to LongC0VID. Worth your time! ➡️EBV, carried lifelong by ~95% of adults, toggles between lytic replication and programmed latency, reprogramming B cells to evade immunity and disrupt homeostasis, ➡️EBNA-1 is central( EB virus-nuclear antigen-1), “The Achilles’ Heel of EBV,” ➡️Via molecular mimicry it cross-reacts with GlialCAM (MS), keratin (RA), and nuclear antigens (SLE), ➡️A "bystander activation" and "epitope spreading" can amplify inflammation in Crohn’s disease, type 1 diabetes, and IgA nephropathy, ➡️EBV also drives lymphoproliferative disease in both immunocompetent and immunosuppressed hosts. "When a usually EBV-negative lymphoma turns EBV-positive, that is often a red flag for underlying immune failure," ➡️Two paediatric emergencies get special attention: - EBV-HLH: A cytokine-storm catastrophe from failed cytotoxicity, - Chronic active EBV disease (CAEBV), - Both can kill, ➡️On LongC0VID the review is cautious: ➡️Separate studies suggest COVID can wake latent EBV in B cells: - EBNA1 mimicry, atypical B-cell expansion, and cytokine dysregulation could then sustain the same inflammatory loops seen in MS, SLE, and RA. - SARSCoV2 would not need to persist, it would only need to reactivate the most omnipresent human virus and let it keep “burning.” - That, according to this review, remains a hypothesis, not yet a settled mechanism, ➡️The authors further argue that mapping these molecular interactions is essential for vaccines and targeted therapies that finally treat EBV as a systemic pathogen rather than a childhood inconvenience, ‼️So, a virus shrugged off as “kissing disease” is a plausible architect of autoimmunity, lymphoma, paediatric cytokine storms, and possibly part of the wreckage after SARSCoV2. Ignoring that possibility is no longer scientifically serious. Sadly, NO licensed EBV vaccine momentarily available. Incoming mRNA candidates are real, but a public shot is not yet imminent! mdpi.com/1999-4915/18/9/1048