What do mummies tell us about the heart health?

Introduction

Atherosclerotic cardiovascular disease (ASCVD) is a leading cause of morbidity and mortality worldwide (1). While atherosclerosis is frequently perceived as a disease arising from the interplay of a Western diet, sedentary lifestyle, and environmental stress, paleopathological evidence suggests that the disease has afflicted human populations for thousands of years. The groundbreaking HORUS study (named for Horus, the ancient Egyptian deity), utilizing whole-body computed tomography (CT) scans of Egyptian mummies spanning up to 4,000 years, demonstrated the unexpected prevalence of atherosclerosis in ancient societies, challenging conventional assumptions about its etiology rooted in ills of modern living (2). Subsequent reports, including the expanded HORUS study of preserved remains from different geographical regions and cultures, ranging from Unangan hunter-gatherers and ancestral Puebloans to ancient Inca from the Peruvian Andes, have further confirmed that this vascular pathology transcended geographical and temporal boundaries (3,4). These findings have conveyed that the atherosclerosis might not be exclusively a modern affliction, and despite presumed disparity in dietary habits, physical activity profiles, environmental stressors, and potential genetic backgrounds, disease manifested consistently in mummies of disparate geographic origins. These studies have allowed a unique window into the behavioral and lifestyle determinants of atherosclerotic vascular disease, even when the availability genetic susceptibility remains poorly understood. CT imaging technology has revolutionized our understanding of the ASCVD and has allowed a unique opportunity to historical presence of atherosclerosis by enabling non-invasive analyses of mummified remains of the ancient civilizations. A documentation of arterial calcification in comparatively younger ancient populations, including a millennium-old South American mummies in thirties and 16^th century Greenlandic Inuit in their twenties (4,5), has confirmed the modern observations that atherosclerosis manifests early in life (6,7). While static postmortem CT evidence of arterial calcification recovered from mummies cannot serve as definitive proof of symptomatic or event-triggered ASCVD, atherosclerotic lesions have been documented in both ancient civilizations and contemporary human cohorts spanning diverse time periods, geographical locales, and genetic ancestries. Two prior comprehensive reviews (8,9) similarly charted the historical progression of atherosclerosis research spanning ancient clinical documentation to contemporary inflammatory pathogenic frameworks, while collating paleogenetic evidence such as ancient human deoxyribonucleic acid (DNA) and Genome-Wide Association Study-derived atherosclerotic risk alleles extracted from ancient specimens. These findings highlight that conventional risk factor-based algorithms are insufficiently accurate to reliably predict an individual’s risk of developing atherosclerosis. Moreover, the contemporary research commonly focuses on advanced lesions poised to trigger acute cardiovascular events (10). This disparity underscores a need for a paradigm shift, from reactive management of end-stage disease to proactive intervention early in the life course and atherosclerosis-guided rather than risk factor-directed therapeutic strategies, toward eradicating the clinical burden of ASCVD.

This review synthesizes archaeological findings with current clinical understanding to explore how can evolutionary evidence inform modern preventive strategy. These interdisciplinary insights not only reshape our understanding of ASCVD origins but also highlight the potential for ancient remains to serve as a longitudinal natural experiment in atherosclerosis progression, offering novel perspectives for contemporary risk stratification and proactive therapeutic strategies to mitigate its burden.

Ancient atherosclerosis: ubiquity across civilizations and implications for modern disease paradigm

Archaeological evidence of atherosclerosis

While atherosclerosis is commonly perceived as a modern lifestyle disease, compelling evidence demonstrates its existence in ancient populations. Pathological examinations dating back to early 20^th century studies (11) and contemporary imaging analyses (2) reveal its presence in mummified remains. The HORUS study of Egyptian mummies, which involved whole-body CT scans of 137 mummies spanning up to 4,000 years (Figure 1), established that atherosclerosis was prevalent even in ancient civilizations (2). The global HORUS study subsequently expanded the sample size to 237 adult mummies from different cultures and continents including ancestral Puebloans from the southwestern United States, ancient fisherman–farmers from the shores of Peru, ancient Andean farmer-pastoralists of Bolivia and Peru, Middle-Ages Mongolian Gobi Desert nomads, and hunter-gatherer Unangan of the Aleutian Islands and Inuit from the shores of Greenland, confirmed that atherosclerotic calcification was present and common in the mummified remains of humans for thousands of years and vast geography (3,4).The Chinese archaeological findings, such as the Western Han Dynasty Mawangdui female cadaver and Southern Song Dynasty mummies from Changzhou, also exhibited evidence of atherosclerotic lesions (13,14). These findings suggest that atherosclerosis has accompanied human civilization for millennia and that its development involves complex interactions among genetic, environmental, and lifestyle factors. Several critical confounders prevent direct one-to-one translation of CT-detected vascular calcification in mummies to clinically significant antemortem ASCVD: first, taphonomic and postmortem mineralization represents a major artifact: long-term desiccation, alkaline burial soils, and Egyptian embalming fluids alter vascular tissue pH and extracellular ion balance, driving secondary calcium deposition within vessel walls independent of in vivo atherogenic processes. Second, mummification induces universal tissue shrinkage, distortion of intimal and medial vascular architecture, and artificial hardening that may exaggerate the volume and density of radiologically visible calcified plaques on CT imaging. Third, unlike living patients evaluated via coronary CT angiography (CCTA), ancient specimens lack correlative clinical metrics: no records of hypertension, dyslipidemia, angina, myocardial infarction (MI), or stroke exist to confirm whether observed arterial mineralization impaired coronary perfusion or triggered cardiovascular death (15). Radiological calcification merely captures static morphological vascular changes at death, rather than dynamic plaque vulnerability, luminal stenosis, or functional ischemia that define clinical ASCVD in modern populations (16).

Figure 1 Computed tomographic evidence of atherosclerosis in an ancient Egyptian mummy. A coronal thick-slab 3D multiplanar reconstruction CT image (vascular calcification window) of the mummy of a male scribe—Hatiay, who died at age 45–50 years, New Kingdom, 1570–1293 BCE, reveals calcific deposits in the coronary and aorto-iliac bifurcation. Calcifications are observed in the proximal and mid right coronary artery, with discernible posterior descending and posterolateral branches distal to these lesions. Courtesy: Greg Thomas MD, FACC, MASNC, Principal Investigator of HORUS team: Atherosclerosis in Evolution. Reprinted, with permission, from Allam et al. (12). 3D, three-dimensional; BCE, before common era; CT, computed tomography.

Despite these study caveats that constrain etiological inferences and preclude direct comparison of lesion burden between ancient humans and modern cardiovascular event risks, the core observation remains unrefuted: vascular lesions morphologically consistent with atherosclerotic mineralization are identifiable across multiple ancient civilizations (17).

Low atherosclerosis burden in pre-industrial indigenous groups

In contrast to pre-modern atherosclerosis research, which predominantly examined mummified remains and identified large-vessel atherosclerosis as prevalent across multiple ancient populations, contemporary studies indicate that certain pre-industrial societies exhibit significantly lower rates of atherosclerosis or reduced coronary risk factors. The Tsimane Health and Life History Project (THLHP) has studied 16,000 indigenous Tsimane individuals in Bolivia, who maintain a pre-industrial lifestyle of hunting, gathering, and farming along the Maniqui River in the Amazon Basin (18). Tsimane population revealed minimal evidence of atherosclerosis compared with any other population studied. Comparative ultrasonography studies from the Heart Attack Prevention Program for You (HAPPY) revealed that a physically active, strictly vegetarian, non-smoking, and meditation-practicing suburban population in India developed carotid and femoral atherosclerosis 15 years later than a demographically matched population in Texas, USA (19).

Atherosclerosis is a multifactorial disease shaped by the interplay between genetic and environmental factors. The unexpectedly high prevalence of atherosclerotic lesions observed in ancient mummies, together with the finding of low atherosclerotic risk among modern pre-industrial populations, serves as a reminder that even combinations of multiple risk factors, genetic predispositions and environmental exposures cannot fully account for the heterogeneous onset and progression of atherosclerosis across individuals. Direct imaging or pathological evaluation of atherosclerotic lesions therefore provides a more straightforward readout of disease status (Figure 2).

Figure 2 Imaging-based coronary CT Phenotyping for heterogeneous atherosclerosis: anthropological evidence, theoretical rationale and clinical implications. Left panel: CT scans of ancient Egyptian and Chinese mummies confirm atherosclerotic calcified plaques existed across distinct ancient civilizations, proving atherosclerosis is an ancient disease. Meanwhile, forest hunter-gatherer populations display minimal plaque burden, demonstrating disease heterogeneity tied to lifestyle. Yellow arrows indicate calcifications detected in both ancient Egyptian and Chinese mummies. Several visual elements in this figure were assisted by ChatGPT(GPT 5.6). The core data, content and underlying concepts expressed in the figure are original work of the author team. Right panel: comprehensive coronary CT phenotyping toolkit including: ① Agatston calcium score; ② stenosis severity; ③ total plaque burden; ④ plaque composition; ⑤ high-risk vulnerable plaque morphologies; ⑥ perivascular fat attenuation index for vascular inflammation; ⑦ CT-FFR to assess hemodynamic significance; ⑧ CT perfusion to detect myocardial ischemia. Middle panel: Conventional risk factor assessment (age, hypertension, diabetes, smoking, LDL-C, obesity) cannot fully reflect actual plaque load and disease phenotypes, as atherosclerosis varies widely biologically and clinically. Modern cross-sectional imaging enables direct, intuitive visualization of arterial plaque and vessel pathology. Standard population-wide risk-factor management yields only generalized risk estimates. In contrast, imaging-guided coronary phenotyping delivers personalized risk stratification and targeted treatment, forming a far more accurate foundation for prevention, risk stratification and therapy. Overall, the figure concludes that anthropological proof of atherosclerosis’s long history and inter-population heterogeneity validates imaging-based coronary CT phenotyping as a modern tool for direct, complete characterization of atherosclerotic burden and phenotypes, enabling precision prevention and individualized cardiac care. CT, computed tomography; CT-FFR, coronary computed tomography-derived fractional flow reserve; FAI, fat attenuation index; LDL-C, low-density lipoprotein cholesterol.

Archaeological discoveries informing contemporary atherosclerosis

Cross-cultural CT imaging of ancient mummies recurrently detects atherosclerotic vascular lesions, proving atherosclerosis is an age-old human affliction rather than a disorder unique to modern disease.

Presence of atherosclerosis in the middle eastern civilization is understandable since the mummification was the privilege of higher stratum of the society who lived in affluence with abundant supply of agricultural and animal products and indulged in limited physical activity to be carried in palanquins. Vascular calcification analysis of ancient biological samples from non-elite populations, i.e., common farming men and women, who lived in Andean foothills and near coastlines—a context presumptively linked to diets abundant in vegetables and fish or lean meat, and ample physical activity. Despite such ostensibly cardioprotective lifestyles, arterial calcification morphologically consistent with atherosclerotic lesions can be identified in relatively young ancient individuals. These findings might be attributed to chronic exposure to biomass smoke from domestic indoor cooking or heating (20), possibly combined with low-grade inflammation induced by recurrent polymicrobial parasitic and bacterial infections (21), both established contributors to endothelial dysfunction and atherogenesis. However, postmortem mineral artifacts cannot be fully excluded as partial contributors to the observed vascular calcification signals on mummy CT scans.

On the other hand, the pathophysiological basis of apparent protection against atherosclerosis in the Tsimane population include favorable profiles of coronary disease risk factors, such as an active lifestyle and diet rooted in subsistence practices, the low-density lipoprotein (LDL) cholesterol levels of less than 70 mg/dL, the blood pressure of <120/70 mmHg, fasting blood sugar of <80 mg/dL, and body mass index (BMI) of <25. This hunting population resides in open huts, does not smoke, eats one-meal a day (OMAD) and walk 15–20 thousand steps a day. Critically, these findings demonstrate that coronary atherosclerosis should largely be preventable in most individuals through healthy living (18). However, it is important to note that 1 of 12 Tsimane individuals, despite their favorable risk factor profile, still developed atherosclerosis, albeit at strikingly lower rates than in industrialized populations (18).

A genetic basis of atherosclerosis has made a convincing contributory argument, when the resolution of risk factors does not completely abrogate ASCVD (22).In the proposal of antagonistic pleiotropy, certain gene variants could confer advantages at early life stages that boost fertility or survival to maturity. Such genetic adaptations subsequently impose detrimental effects, such as elevating disease risks in senescence. The natural selection usually favors alleles with early benefits despite their late-life costs, due to the declining force of selection with age. The evolutionary hypothesis represents one potential explanation for why atherosclerosis-related genetic variants persist in human populations. This pattern was notably confirmed through ancient DNA analysis of Ötzi the Iceman, a 5,300-year-old natural mummy and the 13^th-century Changzhou Mummy, Ji Lizhi, from the Lower Yangtze region in China (14,23). Ötzi carried atherosclerosis-related risk alleles in 104 out of 162 explored loci (64%)–including 58 homozygous and 46 heterozygous risk variants, and Ji Lizhi carried a higher polygenic risk score than 78.5% of modern-day individuals from the global 1000-Genome Phase 3 Project. Interestingly, a landmark study of a 15^th–16^th-century Italian aristocratic mummy demonstrated that elevated nitrogen values, indicative of sustained high animal protein consumption, correlated with severe atherosclerotic lesions observed on radiological imaging (24). Furthermore, isotope analyses across different tissues (e.g., bone, hair, or teeth) enable reconstruction of lifelong dietary patterns, as each tissue type records dietary intake at distinct life-stage. Such multi-tissue approach provides unprecedented evidence linking pre-industrial diets rich in animal products to cardiovascular pathology (25).

As very elegantly established by the Framingham Heart Study (26), atherosclerosis is a multifactorial disease driven by risk factors includes interplay of genetics with dyslipidemia, hypertension, diabetes, and smoking. Subsequent studies have added risk facilitators or risk aggregators to the mix and substantiate the archeological findings of risk promotion. Whereas the INTERHEART study added lifestyle elements such as sedentary behavior, dietary patterns, obesity and stress (27), PURE study added the importance of socio-economic and environmental factors (28). Artificial intelligence (AI) for Healthy Cities further consolidated the risk promoters stratified by communities (29). This understanding underscores the importance of study of evolutionary evidence of atherogenesis with modern tools—not available in earlier times—for development of preventive strategies. The evolutionary evidence of atherogenesis collectively refers to multidisciplinary paleo-anthropological datasets spanning thousands of human civilizations, including: (I) CT imaging-based vascular calcification lesions from globally distributed ancient mummies; (II) paleogenetic risk alleles linked to atherosclerosis retrieved from ancient human specimens; (III) stable isotope and tissue biomarker reconstructions of ancient lifelong dietary patterns; (IV) comparative cardiovascular epidemiological data from contemporary pre-industrial indigenous populations with distinct traditional lifestyles. This multi-layered cross-temporal evidence uncovers the evolutionary origins, multi-factorial drivers and lifelong natural progression of atherosclerotic lesions beyond modern industrial risk models. Since genetic, inflammatory, environmental ancient risk drivers cannot be fully captured by standard laboratory and clinical risk metrics, relying solely on risk-factor prediction models leads to missed detection of subclinical plaque and vulnerable lesions. Direct arterial pathological imaging serves as an indispensable adjunct screening modality. State-of-the-art non-invasive imaging techniques allow direct visualization of atherosclerotic plaques, enabling the in vivo assessment of plaque composition and inflammatory activity for clinical practice and population-based epidemiological studies, thus establishing themselves as robust screening alternatives. Coronary artery calcium (CAC) scoring via CT imaging has been extensively validated as a non-invasive screening tool for subclinical atherosclerosis (30). CAC scores have been extensively validated as robust predictor of cardiovascular risk, with ability to refine risk stratification beyond traditional clinical metric (31).CCTA enables comprehensive morphological and compositional analysis of coronary plaques (32,33). The 2026 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain now provides a Class 1 recommendation for CCTA consolidating its role in evaluation of asymptomatic at risk (34). Multiple CCTA-verified high-risk coronary plaque features including low attenuation plaque (LAP), high plaque burden, positive remodeling (PR) and trans-lesional pressure gradient [change in fractional flow reserve (∆FFR)] are strongly associated with unfavorable outcomes (32,33,35,36). A peri-coronary fat attenuation index (cFAI) has been proposed as a noninvasive means to address plaque inflammation, and hence adverse outcome (35-37).

The advent of semiautomated or automatic volumetric quantifications for LAP [<30 Hounsfield unit (HU) CT attenuation], PR (>1.1), ∆FFR (>0.06) and cFAI (>−70.1 HU) mark a pivotal advancement in CCTA. This approach enhances major adverse cardiovascular events (MACE) risk prediction in stable chest pain patients, as demonstrated in the Scottish Computed Tomography of the Heart (SCOT-HEART) trial (38).Within this trial, LAP emerged as the strongest predictor of fatal and nonfatal MI, outperforming conventional metric including cardiovascular risk scores, CAC, and the presence of coronary luminal stenosis. Notably, even patients with zero CAC exhibited substantial LAP burden (13% had >4 %) in this subgroup wherein 10% of subsequent MACE occurred, underscoring the prognostic value of LAP beyond calcium-based assessments. The cFAI assessment on CCTA has demonstrated that inflammatory cytokines released by diseased vessels inhibit lipid storage in perivascular adipocytes. This pathophysiological alteration manifests as detectable modification in tissue composition, which in turn produce characteristic changes in CT attenuation values. This measurable variation has been validated as a reliable imaging biomarker for localizing and quantifying peri-coronary inflammation compared to non-inflamed fat (37,39). Growing evidence from global studies underscores the clinical significance of cFAI as a prognostic marker across diverse populations, even in individuals without detectable atherosclerosis.

Paradigm shift: prevention, early detection and imaging-guided therapy

Current clinical trials and mechanistic research predominantly focus on advanced atherosclerotic plaques, those either stably stenotic or imminently at risk of MACE. This emphasis drives clinical guidelines toward aggressive treatments initiated only after an established disease, which is often too late (40),and highlights a need to pivot from reactive management to proactive prevention. More importantly, archaeological evidence of atherosclerosis and the low atherosclerotic burden observed in pre-industrial indigenous populations further underscore the substantial heterogeneity of atherosclerotic disease. Multiple uncharacterized risk factors independent of conventional cardiovascular risk factors—including hypertension, diabetes mellitus, dyslipidaemia and tobacco smoking—may drive atherosclerotic initiation and modulate divergent disease trajectories. Consequently, conventional risk models fail to fully explain interindividual variability in susceptibility or resistance to atherogenesis. Traditional cardiovascular screening relies on multivariable risk prediction algorithms and clinical symptom assessment to inform preventive interventions such as lipid-lowering pharmacotherapy and downstream diagnostic workup. As a standard clinical practice, asymptomatic individuals classified as low-risk are frequently reassured without additional vascular imaging assessment. Contemporary research indicates that this risk-stratified framework, which originates from population-level epidemiological studies correlating elevated ASCVD risk scores and symptomatic ischaemia with heightened cardiovascular event risk, carries critical limitations: it may miss vulnerable at-risk subjects, given that a large proportion of patients exhibit discordance between their actual atherosclerotic burden and predicted risk profiles (40).

These observations collectively highlight that atherosclerosis management demands a paradigm shift away from risk-factor-only assessment toward direct evaluation of arterial pathology itself (Figure 2) (41). Aligned with this concept, the recently published Lancet Commission (42) dedicated to redefining coronary artery disease (CAD) advocates a fundamental clinical shift: moving beyond the singular focus on myocardial ischaemia toward a comprehensive, life-course framework centred on atherosclerotic plaque across all its developmental stages.

Early detection and effective imaging-guided prevention of atherosclerosis require robust screening strategies to risk-stratify susceptible populations that must be amenable to direct detection and dynamic characterization of atheromatous plaques. The integration of AI with advanced cardiac imaging techniques may provide transformative solutions to address these clinical challenges (43). Clinical trials including Scottish Computed Tomography of the Heart 2 (SCOT-HEART 2) are actively investigating the efficacy of detecting and treating subclinical atherosclerosis before the onset of overt cardiovascular disease manifestations (44). This randomized controlled trial of 6,000 individuals at risk for CAD is testing whether CCTA-guided management will be associated with better targeted intervention and result in fewer MACE than the current standard of care using cardiovascular risk scores. The study, which began recruitment in 2020, has a primary endpoint of the composite of coronary death or nonfatal MI, with participants followed for 5 years; study is expected to be completed in 2027. Beyond the evolving emphasis on atheroma characterization, next-generation diagnostic paradigms would integrate multimodal biomarkers (45-47) including polygenic risk profiles with AI-derived predictive modeling (48). Such integration should enable quantitative estimation of adverse event probability by correlating imaging phenotypes with genomic and clinical datasets.

Opportunistic screening leveraging routine imaging data represents a promising strategy for cardiovascular risk stratification. AI-driven segmentation of chest CT scans originally acquired for lung cancer screening or other diagnostic indications can now extract quantitative biomarkers of coronary inflammation and plaque burden, demonstrating high prognostic value in recent clinical trials (49). Notably, mammographically detected breast arterial calcification (BAC) correlates strongly with systemic atherosclerosis burden and CAC scores, providing incremental prognostic information independent of traditional risk factors (50,51).

Future directions

The advances in imaging biomarkers and refinement of established ones will significantly bridge paleoradiological, paleopathological, paleogenetic, and paleonutritional information. For instance, analysis of the 13^th-century Changzhou mummy Ji Lizhi (14) exemplifies this integrated workflow: first, paleonutritional carbon and nitrogen isotopic biomarkers reconstruct lifelong dietary animal protein and lipid exposure. Second, paleogenetic polygenic risk scores derived from ancient DNA quantify inherited atherosclerotic susceptibility independent of external lifestyle factors. Third, paleopathological residual inflammatory biomolecules measure cumulative chronic inflammatory burden driven by recurrent infection and indoor biomass smoke, two conserved ancient atherogenic triggers. Fourth, paleoradiological CT biomarkers (calcification volume) quantify the final phenotypic outcome of combined genetic, dietary and inflammatory exposures. Furthermore, machine learning models fuse these four layers of paleo-biomarkers to map causal exposure-plaque relationships across thousands of years of human evolution; this unified paleo-atlas can then be overlaid onto modern multi-omics, CCTA and clinical biomarker datasets to refine contemporary risk stratification. Importantly, archaeological discoveries will continue to provide insights into the evolution of atherosclerosis, refining our understanding of the disease etiology and informing contemporary diagnostic and therapeutic strategies. Mummy paleoradiology confirms arterial calcification captured by modern CAC scoring is a consistent lifelong marker of atherosclerotic burden (12), while widespread young-onset vascular lesions in ancient specimens demonstrate atherogenesis initiates decades before clinical cardiovascular events (52). These evolutionary studies behoove that we must shift the focus from reactive to proactive care, and paleogenetic and paleonutritional data identify hidden high-risk individuals misclassified as low-risk by conventional risk algorithms, who require supplementary CCTA screening to detect pre-calcified vulnerable plaques (low-attenuation plaque, peri-coronary inflammation measured via cFAI) undetectable in static post-mortem mummy scans yet readily detectable using modern clinical population imaging protocols.

The synthesis of paleopathological evidence with contemporary imaging advances demonstrates that atherosclerosis, while ancient in origin, can be tracked to the bud through modern precision medicine approaches that would allow a more accurate risk stratification, and a personalized targeting tailored to individual a patient profile, thereby potentially diminishing the overall burden of atherosclerosis and optimizing long-term patient outcomes.

Conclusions

This review establishes atherosclerosis as an enduring human disease rooted in antiquity, substantiated by paleopathological data recovered from a wide range of ancient civilizations. Nonetheless, substantially reduced atherosclerotic burden has been documented in modern pre-industrial indigenous groups including the Tsimane and vegetarian Indian cohorts. Collectively, these divergent observations illustrate that atherosclerosis develops through intricate gene-environment crosstalk; conventional cardiovascular risk factors alone cannot fully explain interindividual variability in disease onset and progression, rendering direct vascular lesion imaging or pathological examination the most accurate biomarker for evaluating personal atherosclerotic status. Integrating contemporary imaging technologies with evolutionary insights offers a transformative approach to understanding ASCVD etiology, enabling early detection and imaging-tailored personalized prevention strategies. This holistic perspective holds great potential to reduce the global burden of atherosclerosis and improve long-term cardiovascular health outcomes.

Acknowledgments

None.

Footnote

Peer Review File: Available at https://rx.amegroups.com/article/view/10.21037/rx-26-0031/prf

Funding: This work was supported by National Natural Science Foundation of China (grant Nos. 82522047 and 82370513).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://rx.amegroups.com/article/view/10.21037/rx-26-0031/coif). N.D. serves as the Editor-in-Chief of Radiology-X. J.G. serves as an Honorary Editor-in-Chief of Radiology-X. J.N. serves as an unpaid Advisory Board Member of Radiology-X. The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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