17 Matching Annotations
  1. Jun 2021
  2. May 2021
  3. Mar 2021
  4. Feb 2021
    1. Dr. Tara C. Smith. (2021, January 23). A reminder: Especially among the elderly, some individuals will die shortly after receipt of the vaccine. What we need to understand is the background rate of such deaths. Are they higher then in the vaccinated population? We didn’t see that in the trials. Some data from @RtAVM. https://t.co/LJe9k1WJQC [Tweet]. @aetiology. https://twitter.com/aetiology/status/1352810672359428097

  5. Oct 2020
  6. Sep 2020
  7. Jul 2020
  8. Apr 2020
    1. However, a recent pathological study found scarce interstitial mononuclear inflammatory infiltrates in heart tissue without substantial myocardial damage in a patient with COVID-19,13 suggesting that COVID-19 might not directly impair the heart.
    1. Vice versa, we did not observe viral particles in cardiac myocytes and, therefore, we cannot infer on viral cardiotropism. Cardiac myocytes showed non‐specific damage that was mainly characterized by focal myofibrillar lysis. In addition, we did not observe cytopathic endothelia and small intramural vessel inflammation or thrombosis. Other cases are needed to confirm this observation.
    2. Cardiac myocytes showed non‐specific features consisting of focal myofibrillar lysis, and lipid droplets. We did not observe viral particles in myocytes and endothelia. Small intramural vessels were free from vasculitis and thrombosis. EMB did not show significant myocyte hypertrophy or nuclear changes; interstitial fibrosis was minimal, focal, and mainly perivascular
    3. The pathologic study showed low‐grade interstitial and endocardial inflammation (Figure 1A and 1B). Large (>20 μm), vacuolated, CD68‐positive macrophages were seen with immune‐light microscopy (Figure 1C and 1D); they were ultrastructurally characterized by cytopathy, with membrane damage and cytoplasmic vacuoles (Figure 1E). The ultrastructural study demonstrated single or small groups of viral particles with the morphology (dense round viral envelope and electron‐dense spike‐like structures on their surface) and size (variable between 70 and 120 nm) of coronaviruses (Figure 2). COVID‐19 infected Vero cells were used as control. The viral particles were observed in cytopathic, structurally damaged interstitial cells that demonstrated loss of the cytoplasmic membrane integrity (Figure 3)
    1. It is reasonable to expect that severe and critical cases have more severe effects on the cardiovascular system owing to more robust inflammatory response. At this early stage, our knowledge is mainly based on available numerators data, and the exact population-level denominators are not known. Also, it is likely that the asymptomatic and mildly symptomatic cases are missing from most reports, which further skews our understanding of the disease.
    1. There were no obvious histological changes seen in heart tissue, suggesting that SARS-CoV-2 infection might not directly impair the heart
    2. There were a few interstitial mononuclear inflammatory infiltrates, but no other substantial damage in the heart tissue
    1. Heart failure44 (23%)28 (52%)16 (12%)<0·0001Septic shock38 (20%)38 (70%)0<0·0001Coagulopathy37 (19%)27 (50%)10 (7%)<0·0001Acute cardiac injury33 (17%)32 (59%)1 (1%)<0·0001Acute kidney injury28 (15%)27 (50%)1 (1%)<0·0001