UK Study Confirms Long-Term Safety of COVID-19 Vaccine
Headache and fatigue were the most commonly reported incident adverse events of the AZD1222 (ChAdOx1 nCoV-19) COVID-19 vaccine in real-world settings across the United Kingdom; anosmia (loss of smell) and ageusia (loss of taste) were the most frequently reported adverse events of special interest.
METHODOLOGY:
This active surveillance study assessed the safety and utilisation of the AZD1222 COVID-19 vaccine in real-world settings across the United Kingdom between March 1, 2021, and April 6, 2023.
Researchers recruited 17,945 participants (median age, 50 years; 60.4% women; 79.2% White) from vaccination sites, including primary care practices and hospitals.
They collected follow-up data at weeks 1, 4, and 14 and at months 6, 9, 12, and 18 after the initial vaccination through electronic data capture forms to identify recipient-reported adverse events and their incidence.
TAKEAWAY:
Overall, 19,824 adverse events were reported in 6591 participants, which included 399 serious adverse events in 220 participants and 287 adverse events of special interest in 184 participants.
Headaches had the highest incidence rate at 421.28 cases per 1000 person-years (95% CI, 404.88-438.34), followed by fatigue at 386 cases per 1000 person-years (95% CI, 370.46-402.18).
Anosmia and ageusia were the most frequently reported adverse events of special interest. An increased observed-to-expected ratio was noted for anosmia and/or ageusia (39.23; 95% CI, 29.13-49.32) and anaphylaxis (7.38; 95% CI, 2.80-11.95).
During the study period, 11 deaths were reported, with COVID-19 infection being the primary cause for two deaths and thrombosis for one death.
IN PRACTICE:
"This study highlights the requirement for pandemic preparedness, including the ongoing focus on standardising case definitions and producing background rates for AESIs [adverse events of special interest], thereby facilitating the rapid identification of safety signals via Observed versus Expected analysis," the authors wrote.
SOURCE:
This study was led by Alison Evans, Drug Safety Research Unit, Southampton, England. It was published online on May 02, 2025, in BMJ Open .
LIMITATIONS:
The study population showed demographic imbalances, with the underrepresentation of older adults and ethnic minorities. A significant loss to follow-up occurred at each timepoint, potentially leading to underreporting of longer-term outcomes.
DISCLOSURES:
This study was supported by AstraZeneca UK Limited. The authors reported having no competing interests.
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Excluding Russia and Georgia, TOPCAT was positive with a HR of 0.82 and a confidence interval of 0.69-0.98. I think this is a really important point. Ok, now to the EuroPace paper. The problem with studying HFpEF is it is diverse condition — unlike HFrEF. The authors, mostly EP docs, were interested in AF effects in HFpEF. Specifically, whether AF is simply a marker for advanced CV disease or is it an independent risk factor. They made two groups: Study patients who had AF before or at study entry. This was the 'any AF' group. Study patients with ongoing AF who had it at entry. Then they propensity-matched patients with no AF and looked at outcomes. I know, it's pretty easy to predict what will happen. Before I tell you the results, I hope you are thinking: small, hyperdynamic, noncompliant left ventricles are not going to do well with losing the atrial kick when AF occurs. The primary outcome of these comparisons was CV mortality. About 580 patients in TOPCAT who had any AF and 400 had ongoing AF. And they found that: Any AF was associated with a statistically significant increase in CV hospitalization, HHF, and progression of HF. Any AF, however, was not associated with an increased risk of sudden death. Ongoing AF was associated significantly with CVD, pump failure death, CV hospitalizations, and HHF. It was interesting to me that neither any AF or ongoing AF was not strongly associated with sudden death. AF seemed to associate mostly with progression of HF or pump failure. This paper has a lot of complicated comparisons, but I think it can be summarized as AF is a bad thing to have with underlying HFpEF. The question of course, the clinical question, is how to modify this problem with therapy. My first recommendation is to phone-a-friend: your EP colleague. I can't give you a generic right answer because there isn't one. HFpEF patients often have serious comorbidities that have to be considered, things like polypharmacy and CKD and valvular HD and frailty. Maybe antiarrhythmic drugs are the right answer. Maybe ablation. And underused in some places is the 'pace and ablate' strategy. We see a lot more HFpEF these days, because people live longer and with more chronic illness. When AF occurs, it's serious. Take Mr. Rogers' advice and realize that we all need helpers in our lives, and please: call your EP friends.
