1) 2020 JAMA Cardiology study (Puntmann et al.) revealed the devastating cardiac toll of COVID. On advanced MRI, a staggering 78% of recovered patients had heart abnormalities & 60% had ongoing inflammation, regardless of initial severity.
2) Dr. Puntmann's upcoming "myoflame" study is set to reveal further devastating insights into post-COVID heart damage, focusing on microvascular dysfunction, fibrosis, & resulting diastolic dysfunction, pathologies often invisible to standard diagnostics.
3) The danger of LongCovid persists silently. A J. of Nuclear Medicine study found devastating heart & lung inflammation up to a year post-infection, critically, this was found even when patients' standard medical tests returned completely normal results. mountsinai.org/about/newsroom…
4) (2025) This hidden inflammation was only uncovered using advanced PET/MRI imaging. A shocking 57% of patients showed inflammatory damage to the heart muscle, pericardium (the sac around the heart), valves, and major blood vessels like the aorta.
5) Further proof (2025): 58% of LC patients with cardiac symptoms had abnormal Cardiac MR scans, with 43% showing signs of tissue damage (LGE). Relying on standard tests is not enough. Advanced imaging is crucial to unmask this devastating chronic risk.
6) (2021) The COVERSCAN study (Dennis et al.) provides alarming data: Even in "low-risk" individuals w/ persistent symptoms, 70% show signs of organ impairment 4 months post-infection. 29% have multi-organ damage.
7) (2023) The damage is often persistent. A 1-year follow-up study in Open Heart (Roca-Fernandez et al.) shows: Of Long COVID patients with initial cardiac MRI abnormalities, a staggering 58% still had abnormal findings at 12 months. pubmed.ncbi.nlm.nih.gov/36822818/
8) The insidious part: Standard blood tests often fail. The Roca-Fernandez et al. study found 101 patients with NORMAL cardiac blood work (Troponin etc.) who still had pathological findings on heart MRI. This damage frequently goes undetected.
9) Once again confirmed: Standard blood tests are failing. The IMPRESSION study (Puntmann et al.) is clear: Although 73% of participants with mild COVID reported cardiac symptoms and had inflammatory changes on MRI, significantly elevated troponin levels were rare.
10) This confirms the damage from Long COVID often occurs without classic warning signs in the blood.
A frequently overlooked diagnosis is acute pericarditis (inflammation of the heart sac).
11) A study in the Int. Journal of Cardiology (Dini et al.) found this in 22% of the Long COVID patients they studied. It was often associated with palpitations and a history of autoimmune disorders.
12) We made a fundamental mistake framing LongCovid as a single syndrome. While many focused on MECFS, a silent pathology took hold. This isn't just about lingering symptoms; it's measurable organ injury,from myocarditis to pericarditis,that standard blood tests consistently miss
13) This isn't a prediction; it's a diagnosis of what's to come. The widespread, often-silent damage to hearts, vessels, and other organs is seeding a tsunami of chronic illness, from heart failure and pericarditis to autoimmune disorders. We must prepare for this now.
14) The heart was the warning shot. Its hidden damage, invisible to routine tests, foreshadows a systemic crisis affecting all organs. But the true scale of this problem remains unknown until we confront the elephant in the room: SilentLongCovid in those with no symptoms at all.
1🅱️) How do you make a public health crisis disappear? First, you deny the suffering. When that fails, you declassify the event to downplay it. Fragmenting Long COVID is a masterclass in this political strategy. Here’s the 3-step process. A thread:
2🅱️) Step 1: De-link the effect from the cause. By calling post-COVID organ damage a "complication," you sever its tie to the pandemic. A heart attack is no longer a public policy failure: it's a personal tragedy. The system is absolved.
3🅱️) Historically, this strategy has been used many times: When it became clear in the 1950s that cigarettes cause cancer, the tobacco industry fragmented the research to sow doubt. Decades later, this very tactic delayed political action.
1) A new study analyzes immunoglobulin complexes from patients with ME/CFS and a Long COVID cohort who also meet ME/CFS criteria (PCS-CFS). Proteomics reveals they have fundamentally different molecular signatures, suggesting distinct pathologies. A thread on the findings.
2) The key commonality: When applied to healthy human endothelial cells (the lining of blood vessels) in vitro, antibodies (IgG) from BOTH patient groups induced significant mitochondrial fragmentation. This points to a shared autoimmune attack on cellular energy infrastructure.
3) Importantly, this effect appears specific. IgG from patients with Multiple Sclerosis (MS), another autoimmune condition, did not cause the same mitochondrial fragmentation in the lab setting. This suggests the mechanism isn't a general feature of all autoimmunity.
1) Study finds healthy lab-grown muscle exposed to ME/CFS or Long COVID blood quickly loses strength, temporarily boosts metabolism, then undergoes mitochondrial and structural collapse with prolonged exposure. Distinct metabolic and structural differences separate ME from LC.
2) ME/CFS muscles show heightened oxygen consumption and tissue remodeling focused on extracellular matrix repair, while Long COVID muscles rely on mitochondrial compensation but suffer from inefficient energy use and faster fatigue.
3) Despite shared symptoms, ME/CFS and Long COVID trigger unique molecular muscle responses. This reveals they are separate diseases rather than identical conditions, requiring personalized diagnostic and therapeutic strategies.