I’ve done something a little unusual. As a clinician with years of experience treating real people—not models or graphs—I decided to use artificial intelligence not to build a narrative, but to dismantle one.
Recently, I took a close look at a Swedish nationwide study published in the European Heart Journal. It analyzed over 8 million people and seemed to deliver reassuring news: COVID-19 vaccination reduced the risk of serious cardiovascular events like heart failure, stroke, atrial fibrillation, and heart attacks. The conclusion? Aside from a transient risk of myocarditis and pericarditis, the vaccines were not just safe—they were seemingly protective.
Xu, Yiyi, et al. "Cardiovascular events following coronavirus disease 2019 vaccination in adults: a nationwide Swedish study." European Heart Journal 46.2 (2025): 147-157.
But here’s my question: does this match what we're seeing in the real world?
If these vaccines were truly reducing heart failure and heart attack risk, why are hospitals still full? Why do we keep hearing stories of people—many young—collapsing suddenly? Why has there been a persistent rise in ambulance callouts and cardiac-related deaths in highly vaccinated regions?
Let me walk you through what I did.
The Swedish Study’s Problem: An Implausible Baseline
The study tracked vaccine-related outcomes over a 6-week window after each dose. That’s standard in vaccine research. But here's the issue: the authors reported that heart failure risk dropped significantly in those 6 weeks. Not just after one dose—but after all three.
To any practicing clinician, that should raise a red flag.
Heart failure doesn’t magically improve in six weeks—especially not because of an immune response to a vaccine. If anything, post-vaccine myocarditis could worsen cardiac output. So how could the vaccine protect against it? It doesn’t add up.
