Abstract
Dear Editor,
We read with great interest the study by Bolgen and Celik, 1 which reported that aortic arch calcification (AAC) and adverse aortic arch morphology (AAM) on computed tomography angiography (CTA) were independently associated with major adverse cardiovascular events (MACE). The authors are to be congratulated for highlighting the potential prognostic relevance of vascular findings that are frequently encountered yet may receive limited attention in routine clinical practice.
Beyond demonstrating these important associations, an important question is whether aortic arch imaging may provide incremental clinical information beyond conventional risk factors and data already obtainable from cardiac CTA. In many patients in this cohort, coronary plaque burden, obstructive coronary artery disease, and coronary calcium may also have contributed to future risk estimation. Considering these established CTA-derived variables in future analyses may help clarify whether AAC and AAM offer distinct prognostic value or largely reflect a broader systemic atherosclerotic phenotype. Such clarification would be particularly helpful for clinical translation.
Another relevant question is whether incorporating findings from the aortic arch could improve patient-level risk classification. Hazard ratios are valuable for demonstrating associations, but contemporary prognostic studies increasingly also assess discrimination, calibration, and reclassification metrics when evaluating potential clinical utility. 2 In this context, the practical significance of reporting AAC or complex plaque morphology may depend not only on statistical association but also on whether these findings meaningfully influence preventive strategies, follow-up intensity, or downstream testing.
The findings regarding the modified Glasgow Prognostic Score are likewise of interest. The absence of independent prognostic significance in multivariable models should perhaps be interpreted cautiously rather than as evidence against an inflammatory contribution to plaque vulnerability. A single baseline composite of C-reactive protein and albumin may not fully capture the chronic and dynamic nature of residual inflammatory risk. Recent cardiovascular literature suggests that serial biomarker assessment or pathway-specific inflammatory markers may provide complementary insights in this setting. 3
Finally, the study underscores an increasingly relevant concept in cardiovascular imaging: structural plaque burden and biological plaque activity are related but not identical.4,5 CTA-defined calcification and morphology provide important anatomical characterization, though they may not fully reflect lesion activity, thrombogenic potential, or ongoing vascular inflammation. 6 Future multimodal approaches that integrate anatomical imaging with biological markers may further refine the identification of patients at the highest near-term risk.
In summary, this valuable study supports greater attention to aortic arch findings on routine CTA. An important next step will be to determine the extent to which these markers reflect systemic vascular disease versus provide additional information that may enhance individualized cardiovascular prevention.
