Post 1.
Published February 16, 2022, in “Vaccines” (MDPI), this systematic literature review by Maiese et al. examined published cases of death following administration of EMA-approved COVID-19 vaccines up to November 2021.
It identified 55 temporally associated deaths from 19 papers (case reports and small series), excluding anaphylaxis, preprints, and non-English articles. Of these, authors of the source papers excluded causality in 17, left 8 unspecified, deemed 15 possible, 1 probable, and 14 very probable/demonstrated. The standout signal was vaccine-induced immune thrombotic thrombocytopenia (VITT, 32 cases, heavily tied to adenoviral vector vaccines like AstraZeneca’s Vaxzevria), alongside myocarditis (3 cases), and scattered others like ADEM, rhabdomyolysis, and myocardial infarction.
The paper concludes that fatal events are scarce, benefits outweigh risks, and the scientific community must stay unified in promoting vaccination. This framing reflects the era’s urgency, but a closer, evidence-driven examination reveals deep structural flaws that erode confidence in its reassurances and raise serious questions about accountability for harms.
Core Methodological and Evidentiary Weaknesses
This is not robust epidemiology, active surveillance, or controlled data; it is a review of voluntarily published case reports. Such sources are inherently prone to selection and publication bias. Unusual or dramatic cases (young patients, atypical thrombi) are more likely to reach journals, while routine deaths in elderly or comorbid individuals may go unreported or unpublished, especially amid institutional pressures against anything perceived as undermining uptake. The authors themselves note researchers might feel “inhibited” from reporting vaccine-linked deaths due to fear of being labeled anti-vaccine, yet proceed as if the 55 cases fairly represent reality.
The search was limited to major databases through late 2021, missing low- and middle-income country data where billions of doses were administered under different conditions, genetics, comorbidities, and reporting capacities. This creates a high-income skew that cannot speak to global risks. Passive systems (literature, VAERS-like databases) notoriously under-capture serious events; estimates often range from 1–10% for significant harms, rendering “rarity” claims unreliable without robust denominators adjusted for age, sex, comorbidities, and background event rates.
Temporality does not equal causality. Many cases involved older patients with pre-existing cardiac disease, hypertension, or other risks where myocardial infarction, pulmonary embolism, or stroke are common. Without rigorous controls comparing vaccinated vs. unvaccinated populations in similar time windows, excess risk remains speculative. COVID infection itself drives similar pathologies (thrombosis, myocarditis), complicating attribution.
Gaps in Causal Understanding and Investigation
The paper repeatedly highlights unknowns: the precise mechanism triggering anti-PF4 antibodies in VITT (resembling heparin-induced thrombocytopenia but vaccine-linked) is not fully elucidated. For myocarditis, ADEM, and rhabdomyolysis, explanations default to vague “immune-mediated” processes without definitive biomarkers distinguishing vaccine etiology from coincidence or infection. Many cases lacked full autopsies, advanced histology, or standardized adjudication, leading to subjective causality assessments across source papers.
Post-mortem investigations were inconsistent. The authors call for more autopsies, which is telling, as these are essential for clarifying mechanisms in sudden deaths. Later autopsy series (post-2022) have identified patterns of spike protein-related inflammation and thrombosis in some vaccine-associated fatalities, underscoring how this early review captured only a fraction of potential signals.