Les scores élevés de calcium coronaire sont-ils mauvais pour les athlètes d'endurance ?
Le paradoxe de l'athlète : le paradigme clinique du score calcique coronaire : évaluation du risque chez les populations asymptomatiques
Le paysage de la cardiologie préventive a subi une profonde transformation avec l'émergence de l'imagerie subclinique, en particulier la quantification de score calcique coronaire. Depuis des décennies, l'évaluation du risque cardiovasculaire reposait presque exclusivement sur des modèles probabilistes dérivés de données observationnelles à l'échelle de la population. Bien que des outils tels que le Score de risque de Framingham et le Équations de cohorte regroupées ont fourni une base pour prévention primaire, elles restent des mesures indirectes du risque, estimant la probabilité de la maladie sur la base de marqueurs de substitution comme cholestérol niveaux et tension artérielle. L'intégration du score CAC dans la pratique clinique représente un virage vers une approche fondée sur la maladie, où la visualisation directe de la charge athérosclérotique permet une stratification du risque hautement individualisée. Dans la population générale, la présence et l'étendue du calcium coronaire constituent un indicateur robuste et facteur prédictif indépendant du futur infarctus du myocarde et la mortalité cardiovasculaire.¹ Cependant, un nombre croissant de données probantes a mis en évidence un phénomène contre-intuitif chez les athlètes d'endurance vétérans : ces individus, qui possèdent souvent des capacités supérieures aptitude cardiorespiratoire et une mortalité globale plus faible, présentent fréquemment des scores calciques coronariens plus élevés et davantage de coronaropathies plaque que leurs pairs sédentaires.² Ce rapport explore les fondements techniques du score CAC, sa performance prédictive dans la population générale, les mécanismes biologiques proposés pour expliquer le paradoxe athlétique, et son utilité comparative par rapport à d'autres méthodes modernes prédiction des risques Outils.

Fondements techniques du score calcique coronaire
Coronarien artère Le calcium (CAC) est un marqueur hautement spécifique des coronaires athérosclérose et un substitut pratique pour l'ensemble des coronaires charge athéromateuse.¹,³ The development of plaque calcifiée dans le artères coronaires is an active, regulated biological process rather than a passive accumulation of minerals. It typically reflects more advanced phases of the atherosclerotic cascade and correlates with total plaque burden in the epicardial coronary arteries.¹,³ Because calcification reflects only a portion of total atherosclerosis, the presence of detectable calcium generally implies a larger underlying burden that can include both calcified and non-calcified athérome.¹,³
Mechanics of Computed Tomography and the Agatston Method
The standard method for assessing coronary calcium is through non-contrast, electrocardiogram (ECG)-gated tomodensitométrie (CT) of the chest. To ensure high-quality imaging and minimize motion artifacts from the cardiac cycle, scans are typically acquired during a single breath-hold using prospective ECG triggering.³ This synchronization allows the scanner to capture images primarily during diastole, when the heart is most still.³ Modern multidetector computed tomography (MDCT) systems have largely replaced earlier electron beam computed tomography (EBCT) due to their widespread availability and high résolution spatiale.³
The quantification of coronary calcium is most commonly achieved through the Score d'Agatston, a semi-quantitative method originally described in 1990.³ To be classified as a calcified lésion, a coronary focus must typically have an attenuation of ≥130 Hounsfield units (HU) and an area of ≥3 contiguous pixels (≈1 mm²) on standard acquisition parameters.³ The Agatston score for a single lesion is calculated by multiplying lesion area by a weighted density factor based on peak attenuation within that lesion: a factor of 1 for 130–199 HU, 2 for 200–299 HU, 3 for 300–399 HU, and 4 for ≥400 HU.³ The total Agatston score is the cumulative sum of scores across the left main, left anterior descending, circumflex, and right coronary arteries.³ While other measures such as calcium volume and mass scores exist, major clinical guidelines and the bulk of outcome evidence continue to prioritize Agatston scoring for routine preventive risk assessment.⁴,⁵
Safety, Cost, and Incidental Findings
Radiation exposure from CAC scanning is generally low, but varies by scanner and protocol. Estimates for CAC screening radiation dose and associated risk have been published, and typical contemporary protocols are often cited around ~1 mSv under optimized conditions.⁶ The field of view includes portions of the lungs, mediastinum, and upper abdomen, so extracardiac incidental findings are not uncommon and may drive downstream testing depending on local reporting practices.³,⁵
Predictive Accuracy and the “Power of Zero” in the General Population
The clinical utility of CAC scoring has been established through large longitudinal cohorts including the Étude multiethnique de l'athérosclérose (MESA), supporting CAC’s ability to refine risk beyond traditional factors.⁷

The Prognostic Impact of a Zero Score
A CAC (Agatston) score of 0 indicates no detectable calcified plaque and is associated with very low short- to intermediate-term event rates in many asymptomatic adults, often supporting downward risk reclassement in appropriate contexts.⁴,⁵,⁷
Why “CAC = 0” can still miss plaque (the key percentages)
CAC detects calcified plaque, not plaque non calcifiée. In symptomatic cohorts evaluated with angioscanner coronaire (CCTA), clinically meaningful plaque can exist despite CAC=0.
Dans Registre CONFIRM analysis of symptomatic patients undergoing CCTA, among those with CAC=0, 13% had nonobstructive CAD, 3.5% had ≥50% sténose, and 1.4% had ≥70% stenosis.⁸
In a large symptomatic étude de cohorte focused on CAC=0 patients undergoing CCTA, 25.28% had any plaque and 9.32% had obstructive CAD.¹⁰
Age materially modifies the “rule-out” value of CAC=0, with younger symptomatic patients more likely to have non-calcified disease.⁹
These findings are the practical reason CAC=0 should not be interpreted as “no coronary disease,” particularly when symptoms are present.
Risk Reclassification and Ethnicity
Traditional calculateurs de risque provide population-based estimates and may misclassify individuals. Adding CAC can improve discrimination and reclassification, especially among patients initially categorized as borderline or intermediate risk.⁴,⁵,⁷
The Paradox of the Endurance Athlete: High CAC in Highly Fit Individuals
The relationship between exercise and heart health is not purely linear. Cardiac imaging studies of athlètes masters (often defined as individuals >35 years with years of high-intensity training) have shown that some long-term endurance athletes have higher CAC prevalence and/or greater plaque burden than risk-factor–matched controls.²
Research from the Master@Heart Cohort
Dans Étude Master@Heart, lifelong endurance athletes demonstrated higher coronary atherosclerosis burden compared with controls, emphasizing that increased fitness does not uniformly equate to lower measured plaque burden on imaging.² This has contributed to “U-shaped” or “reverse J-shaped” hypotheses proposing that while moderate exercise is protective, very high lifetime training volumes may be associated with increased subclinical coronary atherosclerosis in some individuals.²

Plaque Phenotype, Fitness, and Event Rates
A key paradox is that despite higher CAC in some endurance athletes, many studies observe favorable outcomes influenced by high cardiorespiratory fitness and overall risk-factor profiles.⁴,¹¹ Still, a high CAC score in an athlete should be interpreted as evidence of underlying atherosclerosis requiring clinical attention and individualized risk discussion—not dismissed as “benign athletic calcification.”²,¹¹
Comparative Analysis: CAC vs. Other Risk Prediction Tools
CAC complements traditional risk scores by providing a direct, disease-based measure. Guidelines support CAC particularly when treatment decisions (e.g., statine initiation) are uncertain in borderline/intermediate-risk patients.⁴,⁵ CCTA directly visualizes both calcified and non-calcified plaque and is therefore better suited to symptomatic evaluation and plaque characterization, but is more complex and typically requires iodinated contrast.³,⁹
Future Directions: Photon-Counting CT and AI-Enabled Plaque Quantification
Photon-counting CT (PCCT) is an emerging CT detector technology that can improve spatial resolution and reduce effet de halo, potentially improving calcium quantification and plaque characterization in select settings.¹²,¹³
In parallel, AI-enabled quantitative plaque analysis on CCTA has been evaluated in peer-reviewed studies, including DÉVOILER LA PLAQUE, supporting automated plaque quantification as a step toward more granular anatomic risk assessment beyond a single calcium sum.¹⁴
Conclusion
Le score calcique coronarien is an important tool for cardiovascular risk stratification. By moving beyond statistical probability and visualizing disease burden, CAC enables more individualized primary prevention and prise de décision partagée.⁴,⁵,⁷ Its “power of zero” can identify individuals at very low near-term risk in the appropriate (asymptomatic) context; however, CAC=0 does not exclude non-calcified plaque, and symptomatic patients can still harbor meaningful plaque and even obstructive disease on CCTA.⁸–¹⁰
In masters endurance athletes, CAC highlights a complex reality: some lifelong athletes demonstrate greater plaque burden and higher CAC, but outcomes are influenced by fitness, risk-factor profiles, and plaque characteristics that vary by cohort.²,¹¹ The practical takeaway remains that CAC is best interpreted in clinical context—useful as a risk modifier and decision aid, not as a stand-alone verdict.⁴,⁵
Corrected References
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- Kim KP, Einstein AJ, Berrington de González A. Coronary artery calcification screening: estimated radiation dose and cancer risk. Arch Intern Med. 2009;169(13):1188-1194. doi:10.1001/archinternmed.2009.162
- Bild DE, Bluemke DA, Burke GL, et al. Multi-Ethnic Study of Atherosclerosis: objectives and design. Am J Epidemiol. 2002;156(9):871-881. doi:10.1093/aje/kwf113
- Villines TC, Hulten EA, Shaw LJ, et al. Prevalence and severity of coronary artery disease and adverse events among symptomatic patients with coronary artery calcification scores of zero undergoing coronary computed tomography angiography: results from the CONFIRM (Coronary CT Angiography Evaluation for Clinical Outcomes: An International Multicenter) registry. J Am Coll Cardiol. 2011;58(24):2533-2540. doi:10.1016/j.jacc.2011.10.851
- Mortensen MB, Gaur S, Frimmer A, et al. Association of Age With the Diagnostic Value of Coronary Artery Calcium Score for Ruling Out Coronary Stenosis in Symptomatic Patients. JAMA Cardiol. 2022;7(1):36-44. doi:10.1001/jamacardio.2021.4406
- Yu YT, Hou ZH, Lu B, et al. Prevalence of coronary artery disease in symptomatic patients with zero coronary artery calcium score in different age population. Int J Cardiovasc Imaging. 2021;37(2):723-729. doi:10.1007/s10554-020-02028-8
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- Ramasamy A, Sokooti H, Zhang X, et al. Novel near-infrared spectroscopy-intravascular ultrasound-based deep-learning methodology for accurate coronary computed tomography plaque quantification and characterization. Eur Heart J Open. 2023;3(5):oead090. Published 2023 Oct 30. doi:10.1093/ehjopen/oead090