Dr. Philip McMillan,  John McMillan

Two young athletes died on 1 November. Each death has an explanation on the record, and each points to a question medicine has barely begun to study.

On Sunday, 1 November, Rachel Apa was running her first New York City Marathon, raising money for Parkinson’s research in memory of her grandfather. Early on she texted her father, “I feel amazing.” By around mile 18 the replies had turned to “Ow, ow.” Near the mile 24 marker in Central Park, she collapsed. Despite CPR and a defibrillator, she died in hospital hours later. She was 24, a former Division I field hockey player with no known health problems.

Earlier that day, in a Belfast hospice, Ciara Mageean died of stage 4 bowel cancer at 34. She was European 1500m champion in 2024 and a two-time Olympian.

There is a cruel symmetry to the date. Both families deserve sympathy, and nothing here claims to know what caused either death. But these cases call for a habit of mind every good clinician knows: the differential diagnosis. Beside the most likely explanation, a doctor lists every other condition that could produce the same picture. The most likely answer is where that thinking starts. It should never be where it stops.

What Happened at Mile 24

Her family says doctors blamed rhabdomyolysis. The city’s medical examiner has not yet ruled.

Rhabdomyolysis is the rapid breakdown of skeletal muscle. Damaged fibres spill myoglobin, the enzyme creatine kinase and large amounts of potassium into the bloodstream. Myoglobin can injure the kidneys, but potassium is the immediate danger: a sudden surge can tip the heart into ventricular fibrillation, a chaotic quivering that pumps no blood. There is no pulse. A defibrillator can shock the heart back into rhythm, but while potassium stays high, even repeated shocks may fail.

The mechanism is sound. The timing is the snag. Exertional rhabdomyolysis usually declares itself a day or two after the effort, as creatine kinase climbs toward its peak. A collapse at mile 24 of a November race, far from the summer heat in which the condition classically strikes, does not fit the textbook pattern. Rare is not impossible. So how rare is it? Large studies put cardiac arrest during long-distance races at about one in 185,000 runners.

That is why the list has to be long. Exertional heat illness belongs on it. So does sickle cell trait, a usually harmless carrier state linked to sudden collapse and severe muscle breakdown in athletes. So do dangerously low blood sodium, inherited muscle disorders and silent heart conditions, including old inflammation that left scar tissue behind. An unusually early rhabdomyolysis may be one part of the story rather than all of it.

Scars Too Small to See

That last entry deserves more attention. Since 2020, two triggers of heart inflammation have been well documented: SARS-CoV-2 infection and, less often, COVID-19 vaccination. Either can leave scars.

An analysis of NHS England Hospital Episode Statistics shows myocarditis up 52 percent on pre-pandemic levels, autoimmune pericarditis up 118 percent and acute pericarditis up 30 percent, with acute myocarditis bending upward from 2021.

Japan adds a striking finding. In 2025, pathologists Tomomi Koizumi and Masao Ono described three patients who died in cardiac arrest after episodes of disturbed heart rhythm. At autopsy, their hearts were peppered with tiny, evenly spaced scars, each about a fifth of a millimetre across. In roughly 30 years of clinical pathology conferences, the authors had never seen such scars outside a heart attack. All three had received five or six vaccine doses. The authors could not prove a link to vaccination or infection, and urged that micro-scarring be considered whenever cardiac arrest goes unexplained. Their patients were 73 to 91 years old, a world away from a 24-year-old athlete.

Scars that small are invisible to the naked eye and easy to miss at a standard autopsy. Finding them takes histology, thin slices of heart tissue examined under a microscope. If common, micro-scarring would be a hidden vulnerability, waiting for the day the heart is pushed to its limit. Nobody can say who carries it, because nobody is looking. People who had chest pain or heart inflammation after infection or vaccination would be a sensible place to start.

Stage Four at First Sight

Early-onset bowel cancer has been climbing since the 1990s, long before COVID-19. What sharpens the question now is how it shows up. A cancerous polyp found during a scope can often be removed outright. A cancer that has already reached distant organs is a different disease. In the UK, more than nine in ten people diagnosed at stage 1 survive at least five years. At stage 4, it is around one in ten.

Mageean was diagnosed in May 2025, and her cancer had already spread to her liver and lungs. The first entry on the differential is obvious: delay. Screening and GP appointments were disrupted through 2020 and 2021, and several studies recorded a later shift toward advanced-stage diagnoses. That explains part of the population pattern. Does it explain an elite athlete with a medical team on call?

The Gut Connection

In June 2022, Mageean caught COVID-19 and missed the Irish championships. She later said the illness brought three periods in roughly a month, when her cycle normally ran like clockwork. Such changes were widely reported after vaccination. Here they followed infection, a sign of a strong immune response.

“The patterns of illness are sometimes more important than just the fact that the illness occurred,” said Dr. Philip McMillan, a British researcher and clinician.

Looking back, she said she had dismissed digestive trouble and more frequent trips to the toilet as the kind of thing runners put up with. It took her partner’s insistence and a referral from her Institute of Sport medical team before a specialist in Dublin found the cancer.

The same hospital data show Crohn’s disease up around 48 percent and ulcerative colitis around 73 percent above the pre-pandemic baseline. Long-standing bowel inflammation is an established risk factor for colorectal cancer. And after the nose and throat, the intestine is a favourite home for the virus, which is why SARS-CoV-2 turns up in wastewater.

Then there is CD147, a protein on the surface of many cells. In 2020, researchers proposed it as a back door for the virus beside the usual ACE2 receptor, one that infection itself seemed to widen. The idea is contested: a 2021 study found no direct binding, though other groups reported that CD147 still influences infection. In oncology, its reputation is settled: tumours rich in CD147 tend to be more invasive and more likely to spread. If such cancer cells can be infected, ongoing viral circulation in a heavily vaccinated population could push some early cancers toward aggressive behaviour. Nobody has tested it.

No Evidence, or No One Looking?

The standard reply is that there is no evidence of a link. That is accurate, and it is the predictable result when nobody collects the evidence. A lack of data is not the same as data showing a lack of effect.

The research needed is not exotic. Full histology of the heart whenever a young person dies suddenly during exercise. Studies of how common micro-scarring is in the general population. Cancer registries that record stage at first diagnosis in under-50s alongside infection and vaccination history. Tumour samples tested for CD147 and viral material. Each could confirm the concern or put it to rest.

Neither death proves anything on its own; single rare events seldom do. But a run of rare events among people at the lowest risk ought to shift prior probabilities and send researchers back to their assumptions. Raising these questions days after two deaths will strike some readers as unkind. Waiting a decade for the answer would be unkinder.

“There is still a responsibility to think objectively, ask questions when things don’t fully align, and make sure that there is nothing that we are missing,” said Dr. McMillan.