REF-1578 · De Bosscher et al., 2023 · European Heart Journal · Paper · PubMed

Do lifelong endurance athletes have more coronary plaque?

Yes on scans of men, 191 lifelong vs 176 non-athletes: ≥1 plaque OR 1.86 (1.17-2.94), proximal non-calcified OR 2.80 (1.39-5.65); vulnerable plaque on only 1 vs 6 men, and the authors find composition no more favourable. A plaque is not an event; none were counted. Chest pain, fainting: a doctor.

Main caveat: Cross-sectional endpoint; the authors state a definitive causal relationship cannot be made.
moderate evidenceMeasured on non-athletes and recreational people

The authors hypothesised that lifelong training would go with fewer non-calcified and mixed plaques than a healthy non-athletic life. The data went the other way. Late-onset athletes mostly sat between the other groups. They were significantly above controls only for proximal calcified plaque (OR 1.83, 1.13-2.97) and below them for proximal ≥50% stenosis (OR 0.15, 0.03-0.77).

The authors write that current evidence "cannot relate an increased risk of ischaemic heart disease events" to endurance athletes, and offer possible reasons for the paradox: vulnerable plaques were rare, burden stayed low, and athletes have larger coronary arteries. The authors plan longer follow-up.

Protocol

Athletes: cycling ≥8 h/week, running ≥6 h/week or triathlon ≥8 h/week for at least 6 months. Lifelong began before 30, late-onset after 30. Non-athletes: ≤3 h/week of activity with no prior regular endurance exercise.
Exclusions: cardiovascular disease, diabetes, high cholesterol, hypertension, any smoking history, BMI >27.2.
Sampling: media recruitment; 1152 eligible, 605 sampled at random within age and start-age strata, 47 excluded on the day.
Scan: CT coronary angiography and Agatston calcium, readers blinded. Vulnerable plaque: at least 2 high-risk features.
Funding and interests: Fund for Scientific Research Flanders; interests not in what was read.

Key Results

Median (IQR) or %Lifelong (n = 191)Late-onset (n = 191)Controls (n = 176)Lifelong vs controls, adjusted (95% CI)
Endurance years36 (29-44)14 (9-20)5 (0-26)—
Plaques per person2 (0-5)1 (0-3)0 (0-4)difference 1.1 (0.2-2.0)
≥1 plaque63.4%57.1%50%OR 1.86 (1.17-2.94)
≥1 proximal plaque55.5%45.5%40.3%OR 1.96 (1.24-3.11)
≥1 non-calcified23.6%16.8%15.3%OR 1.95 (1.12-3.40)
≥1 non-calcified proximal16.8%9.4%7.4%OR 2.80 (1.39-5.65)
≥1 mixed29.8%26.2%22.2%OR 1.78 (1.06-2.99)
≥50% stenosis12%4.7%7.4%OR 1.69 (0.78-3.68), not significant
Vulnerable plaque0.5% (1)1.0% (2)3.4% (6)OR 0.11 (0.01-0.98)
A claim stronger than its table. The conclusion speaks of plaques with significant stenosis in lifelong athletes against fit, healthy men. Against controls, stenosis was not significantly different (table above; proximal ≥50%, OR 0.88, 0.32-2.41). The significant contrasts are with late-onset athletes (OR 2.79, 1.20-6.50; proximal OR 5.92, 1.22-28.80).
Reporting. The results text calls plaque number similar across groups, while the table gives 1.1 more (0.2-2.0) and the conclusion says more in lifelong athletes; the adjusted calcium score is not significant (32.1, -14.22 to 78.4), but its percentile and the >0, >10 and >100 cut-offs are. 33 of 191 prints as 16.8% and 37 of 191 as 20.4%; these are 17.3% and 19.4% (our arithmetic). Controls have 5 (0-26) endurance years despite the no-prior-exposure rule.

Mechanisms

Authors' interpretation: a reverse-J dose-response is speculated, drawing partly on a rodent study. Their discussion says that training increases burden and that a healthy lifestyle prevents atherosclerosis; a cross-sectional design cannot show either, as their own limitations say.
Inference: diet (the authors raise high-calorie and high-protein intake), doping (denied, untested) and whatever keeps men training for decades may differ between groups and are unmeasured.

Practical Application

Do lifelong endurance athletes have more coronary plaque? Yes on scans of men, 191 lifelong vs 176 non-athletes: ≥1 plaque OR 1.86 (1.17-2.94), proximal non-calcified OR 2.80 (1.39-5.65); vulnerable plaque on only 1 vs 6 men, and the authors find composition no more favourable. A plaque is not an event; none were counted. Chest pain, fainting: a doctor.
Good for: honesty with a veteran athlete: high fitness does not show clear arteries, and classic risk factors stay worth knowing (Inference).
Not good for: telling anyone to train less. No events, no dose threshold, and the arm with the most plaque also had the fewest vulnerable plaques, on 1 vs 6 men.
Not good for: ordering a scan, or reading one: what a result means for training is their doctor's call. Scanning was not tested as a strategy; REF-1528 says routine preparticipation testing is not required for most asymptomatic individuals.
Symptoms: palpitations, chest pain, fainting: a doctor.

Limitations

Cross-sectional endpoint; the authors state a definitive causal relationship cannot be made.
Surrogate. No events in this report; follow-up continues.
Multiplicity. Intervals were not adjusted, and the authors warn against treating them as definitive.
Questionnaire-based lifetime load; doping denied by athletes, not tested.
Men only, White only; volunteers answering advertisements, though sampled at random after that.
Small counts behind vulnerable plaque and stenosis ORs; power was calculated on mixed plaque by exercise age, not on the many outcomes reported.
How this entry was checked and changed
Why this level

cross-sectional measurement study with n ≥ 100, read from the full text, with random sampling from eligible candidates and blinded readers. It grades a scan finding, an imaging marker; it does not carry evidence about heart attacks or death